SECOND CARNEGIE INQUIRY INTO POVERTY

AND DEVELOPMENT IN SOUTHERN AFRICA

sone diseases associated with poverty

Etlited by Peter Disler Chippy Olver

Carnegie Conference Paper No.295

Cape Town 13 - 19 April 1984 ISBN 0 7992 0754 3 i

PREFACE

It is now nearly 50 years since the then Medical Officer of Health of Cape Town wrote in the SClUth African Medical Journa11• "Poverty is not only a cause of ill health and mortality; it is also a result of them ...... my object is not to discuss the prevention or palliative remedies for poverty, but only to emphasize once more its fundamental relationship to public health." In many ways these perceptive thoughts crystallize the motivation behind this manual. It is not our intention to discuss approaches to the management of poverty, nor to provide a comprehensive text for the medically qualified; neither is this a guide line for people afflicted by both poverty and illness (many of whom would anyway be illiterate by virtue of their economic status).

The target group for this mnaual is the many non-medically qualified persons who work daily with poor people, who encounter illness and who do not have a basic knowledge of the diseases, their frequency and their management. It is hoped that this text will provide some insights which will enable them to deal with the general problems more thoroughly. As many of the diseases covered are based in similar environmental cir­ cumstances, to avoid repitition a general introduction has been provided by Cedric De Beer. This deals with many of the socio-economic factors associated with poverty that influence health in general and in the South African context, in particular. .ii

Selection of the topics for discussion engendered considerable debate. The final list is a rather arbitary combination of the choices of the members of the Carnegie Inquiry health subcommittees in Durban, Johannesburg and Cape Town and based on our joint experience.

Almost certainly there are deficiencies both in the format and selection: important diseases may have been omitted and others inappropriately included. If this booklet proves to be of value then it may deserve expansion and wider distribution in the future and modifications can be made at that stage. Suggestions and constructive criticism will thus be welcomed.

References 1. Higgins, T.S. Public health aspect of social welfare, S Afr Med J 23.9.39, p.p. 675 - 77 iii

INDEX ·Page Number

Introduction Cedric de Beer

Malnutrition Noms(l'ldaba & Chippy Olver 16

Tuberculosis Chippy Olver 27

Diarrhoeal Disease in Young Children Anton van der Merwe

Cholera Anton van der Merwe 43

Sexually Transmitted Diseases Margie Duncan 49

Poliomyelitis Peter Disler 55

. Rheumatic Fever Peter Bundred 60

.. Measles Gerry Coovadia 66

Skin 'Infections Z. Hamed· 73

Tetanus M. Broughton 79

Parasitic Infestation M. Mackenjee 83

Disability and handicap Peter Disler 87

Occupational Lung Disease Derek Yach & Jonny Myers 94

Hypertension Chippy Olver 104

Road Traffic Accidents Noddy Jinabhai 115

Dental (oral) health and disease Hanif MoolIa 127 INTRODUCTION

by Cedric De Beer Department of Community Medicine, University of Witwatersrand, Johannesburg

In the last few decades the introduction of scientific method into medical practice has transformmed it from an art into a sCience. Through medical science, and the other sCientific disciplines on which it draws for its growth and development, we have gained considerable knowledge about the normal functions of the human body, the nature and cause of malfunctions and how this can be corrected. We now know that some infections are caused by bacteria or viruses. We know that the accun·ulation of various substances in the human body, transmitted from the environment or through diet, can cause a number of different disorders. We know that psychological stress can cause physical illenss.

Yet this scientific approach to disease, although bringing many benefits is marked by certain inadequacies. Concentrating as it does on the diagnosis and treatment of individuals, it makes illness appear to be a random event which strikes down those who have been "unlucky" enough to be exposed to a hazardous extrinsic factor. In fact though, we know that this is not the case and that different groups of epople show different patterns of disease. This can be easily domonstrated by looking at statistics describing causes of death in different social classes, ranging from social class 1 (professionals and executives) to social class 5 (unskilled workers). If we compare the causes of death in classes 1 and 5 some interesting patterns emerge. For example in the years 1970- 72, British babies in social class 5 were 2,5 times more likely to die before they reached the age of 1 year than babies born into class 1. Turning to the main causes of death amongst men between the ages of 15-64 further illustrative data is found. Conventionally ischaemic heart disease is regarded as an "executive" disease. This is true in one sense. It is after suicide the most common killer of class 1 males and only the seventh most imnortant cause of death in class 5 males. Nonetheless class 5 males are more at risk of dying from heart disease 2

than class 1 males. Thus not only do members of social- class 5 suffer. from diseases that are not very important for those in class 1, but even those diseases which take the most serious toll ,in social class 1 are more common in class 5. It seems quite clear therefore that socio- economic status does have an influence both on kinds of illness that people have and how frequently they occur.

A similar but exaggerated pattern can be found in South Africa. It is unfortunately impossible to ascertain precisely how great the difference is as there are no adequate health statistics kept for Blacks in this country, except on an extremely selective basis. Nevertheless if this is borne in mind, some important facts emerge from-the available data. In 1970 the infant mortality (number of deaths of children under the age of 1 per 1 000 live births) was 5 times greater amongst Coloureds and Indians than amongst Whites. Even more dramatic was the death rate amongst children between the ages of 1 and 4, being 15 times higher among Coloured children than in White. The significance of these differences becomes apparent if we accept what Van Rensburg and Mans have to say about them : "Infantile deaths are always a reliable reflection of the standard of hygiene and nourishment in a population, its standard of living and health care. Deaths in the age group 1 --4 years reflect the economic and social development of a population rather than the quality of its medical care. ,,1.

As statistics are kept according to race, not class in South Africa it might be argued that these differences are genetically determined and independent of socio-economic status. There are however two strong counter-arguments. The first is that there is in fact an extensive overlap between race and social class in South Africa. For example the Industrial Health Research Group at UCT has argued that 82% of Africans 2 fall into social classes 4 and 5, while only 6% of Whites do. • The second point is that health patterns amongst racial groups change with time. For example the "Asian" population has a lower infant mortality rate at present than it did twenty years ago, and a higher rate of death from coronary heart disease, these changes corresponding with an improvement in the economic status of at least one section of the community. Similarly 3

in the 1920's and 1930's when there was a substantial ''poor White" element, this section of the population showed a pattern of disease similar to Blacks in South Africa today.3. With the almost complete eradication- of real poverty amongst Whites, this pattern of ill health has changed. Clearly, while race and social class are closely linked, the health profile of any group of people changes as their social and economic circumstances change and is not "fixed" by their race."

Once this is accepted, it becomes clear that understanding illness and health is as much a question for social science as it is for medical science and that improving the health of the population (rather than of individual patients) may have more to do with social and economic change that with advances in medical technology. The truth of this 4 statement is aptly demonstrated by McKeown . who showed that a substantial reduction in the incidence of a number,of infectious diseases in the UnHed Kingdom took place years in advance of the development by medical science of the means to treat or prevent these illnesses. McKeown argues that the improvement was the result of changes in the economic and social conditions of the working classes in the United Kingdom which made people less susceptible to the diseases. The importance of these conclusions is that in the analysis of disease, medical principles must be applied to the nature of illness in society as a whole, rather than restricting them to the diagnosis of the disease in the single individual.

Disease and poverty in South Africa

It is beyond the scope of this introduction to examine either the extent or the roots of poverty in this country. These factors will presumably be extensively addressed in other papers presented to this conference. Suffice it to say that in South Africa, and in particular in the "homelands", poverty is both widespread and severe. It is also impDrtant to stress' that poverty is not an original state out of which people must "advance". It is rather a state of deprivation created by the position that groups hold within any particular set of social and economic structures. This concept will be examined in further detail elsewhere in this paper. I 4 r

There are several ways that poverty and disease in South Africa are linked. Al though they are all related, it is worth looking at them separately.

A. Poverty, malnutrition and disease

Malnutrition, and particularly undernutrition, is directly related to poverty. Given that South Africa is a net exporter of food, and that the Black population has not always suffered from the extensive malnutrition that it now does, it is also obvious that this malnutrition is determined neither by geographical nor ethnic factors, but rather by the particular form of social relationships that have developed in South Africa. David Webster, after quoting from a number of, early European travellers in SouthAfrica, draws the following conclusion:5 .

"It is dangerous to generalise about early Southern African societies from the scanty evidence available" but there appears to be consensus on certain'key issues. Most important is the general acceptance by observers that the indigenous population was adequately fed, and were of outstanding physique."

Further, in her paper on malnutrition in the Nqutu district, Liz Clarke, 6 quoting one of these early travellers, notes: •

'~e Zulu diet included meat from periodic feasts, quantities of amasi and a wide range of vegetables, including sorghum, millet, pumpkins, gourds, melons, yams, various tubers akin to the potato, various nuts and indigenous beans, and a wide variety of green herbs and plants. The diet Briant describes is a very different proposition nutritionally to the various forms of porridge which form the almost total diet of so many rural households today."

The situation is very different today. The histor~al processes in South Africa that have led to this change are complex. They involve the transition of a settled rural African population existing as pastoralist­ cultivators to "sub-subsistence rural dwellers, manifestly unable to support themselves by agriculture, and dependent for survival upon wages 5

earned in 'white' industrial regions or on 'white' farms.,J· Colin Bundy describes four main phases in this transition.7.,

1) A well-established pre-colonial subsistence economy existed prior to 1820, infiltrated by missionaries and traders, occurring alongside areas of conquest and annexation.

2) Between 1820 and 1870 colonialism stimulated the emergence of a peasant class, who were capable of producing a surplus for trade purposes.

3) From 1870 onwards a series of Land Acts, culminating in the 1913 Land Act, restricted the African population to 13% of South Africa's land. Taxation was also instituted during this period. The emergent peasantry sank to sub-subsistence level and were forced out as migrant labourers.

4) By 1890 the underdevelopment of the reserves was, already well estpblished, and this has continued to serve a functional role as a supplier of cheap unskilled labour. (,

"The rural population is therefore caught in 'a downward spiral of 'intensified underdevelopment: The absence of the potentially ,progressive young

(as migrants) and the accompanying decline in agricult~r31 productivity means that economic self-sufficiency slips even further away. The balance swings decisively away from home production to reliance on cash remittances from migrants and food bought in the trading stor~." S.

Against this background the dynamics of the family unit assume great importance. The exodus of the adult men as migrants has a major disruptive effect on the 'social system, and on family life. Desertion and illegi~imacy are a direct consequence. Trudy Thomas,8. gives the following approxim­ ations:

60%, of malnourished children are illegitimate 80% of malnourished children have been deserted by their fathers, most of whom are working in' the cities, but do not support their children. 10% have fathers who are sick, unemployed or dead 10% receive support from their fathers. 6

In this context, a recent survey in the Ciskei9• pinpointed family disorganisation as the major factor in influencing the development of mal­ nutrition. Indeed, it appeared more important than either cash resources or the educational status of the mother, the latter having previously , been found to be of relevance in the urban setting. The scenario of ,an absent father and often mother too with the child care relegated to an often inadequate guardian appears to strongly millitate towards mal­ nutrition.

An important element of this J.Illly be early weaning, which is necessitated by the mother leaving home to seek work. The substitution of breast- milk by expensive milk formulae (often widely advertised in the ''homelands'') may have disastrous effects immunologically, nutritionally and in other ways for the child and disrupt the economic balance of the whole family.

Professors Moosa and Coovadia, of Durban Medical School,have calculated that somewhere in the region of 30 000 children die annually in South Africa of malnutrition-related illnesses. These deaths fall into two categories. Firstly there are those who die simply from starvation. In this respect the two major ways ,in which malnutrition expresses itself in children are mainly Kwashiokor and Marasmus. Either of these conditions can kill. However a greater proportion of ~lnutrition-relateddeaths do not result from starvation as such. Rather they occur because the child, weakened by inadequate nutrition, either dies from an illness which would not threaten the life of a well-fed'child, or because the whole body, in a weakened state, contracts a lethal disease against which he/she would otherwise have been adequately protected. For example ~ • a well nourished child who contracts measles is likely to be ill for . a While and then to get better, no worse for the experience. In a poorly nourished child this illness can quite easily progress to pneumonia and death. Similarly, in ,the case of gastroenteritis the well nourished child is likely to emerge none the worse for ~ar while for the under­ nourished child, the disease may be far more serious. With the initial 4isadvantages of lower body weight, decreased recuperative powers',and a generally weakened constitution, the sudden rapid loss of fluid that

-- accompanies gastroenteritis may well tip the balance and kill the child. Even if it does not do so immediately the child's nutritional status is likely to deteriorate significantly during the episode and so render the chances' of surviving even more precarious in the future.

In the case of tuberculosis, good nutrition provides a substantial degree of protection and this most prevalent of all South Africa's major illnesses is most'unlikely to strike a well-fed and otherwise healthy person.

B. Poverty, the environment and ill,health

There are various elements of the social and physical environment that render poor people more susceptib1eto various 'kinds of ailments. This is particularly true in South Africa where poverty is so closely related to race and therefore to national oppression and a .complete absence of political power. This is important, as some of the environmental factors that predispose people to disease are as much related to this lack of political power as they are'to.poverty. For example an adequate supply of clean water and sanitation are fundamental if health is to be preserved, Yet there a,re many millions of South Africans, especially in the "Homelands" who have access to neither. There is nothing "intrinsic in the nature· of poverty that determines that poor people will drink water from springs and rivers; ·or. not 'have,a sanitary sewerage disposal system. It is rather that the same political structures that keep people in rural ghettoes without land or jobs ensure that they will not have the political power to force ,the authorities to provide.them with adequate systems of water reticulation or sanitation. The only direct impact that poverty has on this problem is that if the people concerned had sufficient money

they wou~d be able to purchase at their own cost these services with which .the state is not providing them. The result nonetheless; is that the very poor in South Africa do not have adequate sanitation or. supplies of clean. water and this has a devastating impact on their health, exposing them to a wide range of diseases. 8

The infective organisms that cause gastroenteritis are spread in three main ways, viz. a lack of clean water to drink, inadequate sanitation which allows the spread of faecal matter and insufficient water for washing which also promotes the spread of faecal matter to food and eating implements. Further, the existence of cholera and typhoid as major ha,zards in the "homelands" is directly related to the fact that people need to use polluted water sources. In addition a number of skin diseases, eye infections and other illnesses, which are related to poor hygiene, are prevalent in areas where scarce or polluted water supplies coincide with other predisposing factors to promote the spread of these diseases. Bilharzia is another debilitating illness, the pre- valence of 'which derives directly from people being exposed to infected water sources because of the non-availability of clean water.

The absence of reticulated water does not only mean that the supply is polluted and limited. The water source is also often a long distance from the household. This means that people often spend hours every day walking to the water supply, waiting their turn at the spring and then ,carrying small but heavy quantities of water home. This drastically limits the time available for any form of economic activity which might help to lessen the burden of poverty.

Water and sanitation are largely porblems of the rural areas, but there are still urban townships in South Africa where water is piped to communal taps and where a ~ucket system' of sanitation is used. Infrequent collection of night soil, combined with a tendency for communal taps to be left running, may turn the streets of such townships into relative sewers.

C. Housing, overcrowding and the living environment

Many of the factors already mentioned are exacerbated by other factors likely to be found in the environment of the poor. Chief amongst'these is poor housing and overcrowding. This is one of the dominant features of the South African social environment. Estimates of just how bad 9

the problem is vary, but one in the middle of the range says that in ,.1981 there was a shortage of 160 000 housing units in urban areas and 260 000 units in the rural areas of South Africa. This shortage must inevitably result in overcrowding (up to 17 people in 4 roomed housed in Soweto), squatting in a variety of extremely poorly constructed shanties and straightforward homelessness. 10 •

Clearly, anyone with enough money should be able to afford to build, , buy or rent a home. Similarly, people with very little money may "choose" to live in overcrowded conditions to reduce expenditure on rent. Only in this sense can overcrowding be directly related to poverty. For the rest the housing shortage in South Africa and con­ sequent overcrowding is directly related to various aspects of state policy. This policy has manifested itself ina variety of ways ranging from a decision in 1968 which effectively resulted in a prohibition on the building of housing for blacks in urban areas, to the forced relocation of about 3 miliion people in the last quarter century. This exercise in social engineering has resulted from the implement­ ation' of the Group Areas Act, from Homelands consilidation, from black spot removals, the eviction of tenants from white farms and the operation of' influx control legislation and the pass laws. A considerable number of these forced moves have involved the destruction of already existing housing, and have often forced people into a variety of "informal settle­ ments'" often with very poor shelter and few or no services. 11.

The relationship between housing, and overcrowding, and poor health 12 13 is obvious in some respects. Irwig • quotes Cassel • as follows:

"There can be little disagreement that certain health conditions are directly determined by the physical structure of housing. The relation­ ship of peeling lead paint to lead pOisoning, of dilapidated structures to home accidents, the effects of inadequate heating, broken plumbing systems, the presence of insects and rodents, stagnant water in cellars, and inadequate waste management and disposal are self-evident." 10

Although thers is still debate in this respect, it seems clear that there is some relationship between overcrowding, increased risk of' tuberculosis, rheumatic heart disease and meningitis.

l Irwig goes on !.: "Crowding has also·been found to be associated with an earlier age of occurrence of childhood infections such as measles, whooping cough, diphtheria, mumps, scarlet fever, german measles and chicken-pox. At least for measles, whooping cough and diphtheria, this early age of occurrence is associated with an increased risk of death from the disease."

In other instances, the relationship between health and housing is likely to be more indirect. Overcrowding may interact with other environmental factors to create a new health problem or exacerbate an existing one·. For example in Katlehong township on the East Rand there is a large population of people living "illegally" in shacks at the back of houses. One consequence of this has been to overload the sewerage system in the area. This has resulted in substantial pollution of the area and the creation of major health hazards. The intense overcrowding in some "homeland" villages which have practically no sanitation, means that the quantity of faecal matter lying around increases as does the number of people using inadequate and increasingly polluted water supplies.

Bad housing and overcrowding must also be stress factors in the lives of people who are subjected to these conditions. It is recognised that people under stress are more likely to fall prey to illness of all kinds than people who are not so stressed. In addition the pressure of sharing rooms, the lack of privacy, the lack of adequate facilities and services, the shortage of recreational facilities, and.the threat of violent crime which is associated with poverty, must combine to produce major strains on the psychological wellbeing of the individual. These conditions are reflected in the consequent level of alcoholism, violence and neurotic and psychotic episodes that are 'more characteristic of slums than a middle or upper class neighbourhood •

. ~ ,,

D. Work, unemployment and disease

Almost by definition, the poorest people in a capitalist society are going to be those who are unemployed, and those who are unskilled workers. Both these categories of people are subjected to additional threats to their wellbeing. In the first instance being unemployed, subjects the individual to a wide range of personal and social stresses which will increase his or her susceptibility to disease. Given that there are perhaps three million unemployed people in South Africa, this means a substantial proportion of the population are subjected to these risks. This is aggravated in this country by the "homeland" policy which confines the majority of unemployed people to defined areas with little chance of employment.

Those who are lucky enough to have jobs are subjected in turn to a variety of health hazards. Mainly relatively unskilled workers, for example about one-quarter of a million workers, are injured in accidents each year and 800 are killed annually in accidents in the mines alone. Injury through accident is only one of the threats facing the health of workers. Many workers are exposed to dust, noise, chemicals and other substances, which are harmful over a period of time. Millions of workers are exposed to such substances as ammonia, benzine, lead, asbestos, silica dust and cotton dust. 14.

Finally, it might be noted' that many workers commute for hours to and from work because they are forced by the logic of apartheid to live far from the i'ndustries ar'e located, many in unpleasant township setting, some in single sex ho'stel's, some separ'ated for most of the year from their families. All of these are stressful conditions which at the least cannot be expected to promote the health of those who live under them.

This section has provtded a brief review of some of the elements of the social and physical environment of the poor'which can be expected to undermine the health of the poorest section of the population. It would be misleading to pinpoint one of these elements as most hazardous. 12-

They tend to combine and to be interrelated. Water and sanitation, occupational hazards and poor housing, unemployment and malnutrition, all these factors together form a web of disease prom0ting agents. To be poor in South Africa is truly to be exposed to the threat of ill health and premature "death.

Poverty and Health Services

In all illness-inducing environment, even the very best health services can only be of palliative ;alue. However their absence becomes yet another factor contributing to ill health. Poverty is not in itself a reason why people should receive inadequate health care. If South Africa had an adequate national health service, then health care would be within reach of everyone. Because the state does not provide such a service, poverty. becomes a factor as those without sufficient money cannot afford to go to a private doctor or private clinic. Not sur­ prisingly this situation is worse in the homelands where the governments starved of finance simply cannot afford to provide adequate health care facilities. Indeed KwaZulu for example spends less on hospital services in the whole territory than is spent on one general hospital ·in Johannesburg. The result is that many people live out of reach of any health service at all. Only 3% of practicing doctors in South Africa work in the homelands. White South Africans have a doctor patient ratio of 1 doctor for every 875 people. Bophuthatswana has been estimated to have just more than 2 doctors for every 100000.15 The situation is complicated by the fact that each homeland has its own Department of Health and it seems likely that separate Departments for Coloureds and Indians will soon be set up in the whole of South Africa.

The situation in urban areas is not as bad, but is certainly less than satisfactory. Hospital beds for blacks are in short supply resulting in serious overcrowding in some hospitals and in patients reveiving less than adequate treatment in many circumstances. Moreover, a situation has been created whereby many different authorities are 13

responsible for providing different aspects of health care. All this adds up to a situation where those people who are at risk receive the least adequate care. The result is that various diseases, some of them mass killers, such as measles, which would be entirely prevented with better health care are still common, and that others such as polio break out from time to time.

CONCLUSION

In the tourse of this introduction many different factors have been mentioned which ontribute to the ill health of the poor. By and large these factors do not affect the health of the wealthy. It would however

be incorrect to draw the conclusion that poverty itself ~ ill health. Only malnutrition resulting from the inability to buy adequate food derives from the nature of poverty. The other factors, poor social and health services, an unhealthy living and working environment, inadequate provision of water and sanitation are in South Africa at least, consequences of the same set of social forces that .cause poverty in the first place. As such they are symptoms of the same social disease, racial oppression and economic exploitation as poverty is.

The solution to the health problems outlined in this booklet. ar~ not to be'found in the search for individual cures to the diseases of poverty'. Rather it is to be found in radical changes·in those economic and political structures that cause both poverty and HI health. 14

REFERENCFS

1..Van Rensburg, H. and Mans, A. Profile on Disease and Health Care in South Africa. H & R Academica 1982.

2. Critical Health No.8, 1983.

3. Report of the National ·Health Services Commission UG30, 1944.

4. McKeowen, T. and Record, R. "Reasons for the Decline in Mortality in England and Wales in the 19th Century" in Flynn, M.W. and. Smout T.C. (eds) Essays in Social History, Clarendon Press, 1974.

5. \~ebster, D. The Political Econo~-oof Food Production and Distribution in" outh Africa in Historical Perspective. In Leech Vol. 51 No.2, 1980.

6. Clarke, L. "The Need for a Community Development Approach to Combatting Malnutrition." in Wilson, F. and Westcott, G. (eds) Hunger Work and Health Ravan, 1980.

7. The Emergence and Decline of the South African Peasantry. Colin Burdy, St Anthony's College, Oxford. Published by Kegan Paul in African Affairs.

8. Their Doctor Speaks. Trudy Thomas, 1973. Published by Mary Wheelden.

9. The Social Background of Childhood Nutrition in the Ciskei. G.C. Thomas Soc. Sci. Med, Vol. 15A, 1981.

10. For background on Housing in South Africa see Ruling the Townships published by Labour Research Committee, Johannesburg, 1983.

11. SPP Reports Vols I - V Surplus peoples project Cape Town 1983.

12. Irwig, L.M. A Review of the Relationship between Housing and Health (unpublished paper) •. lS

13. Cassell, J. The Relationship of the Urban Environment to Health : Implications For Prevention. In Mount Sinai Journal of Medicine 40, 1973.

14. Green, P. and Miller, S. "The Commission of Inquiry into Occupational Health", in. Wilson, F. and Westcott, G. Hunger, Work and Health. Ravan Press, 1980.

15. For more information of Health and Health Services in South Africa see forthcoming book, de Beer, C. The South African Disease - Apartheid, Health and Health Services. (title provisional) SAR~ Johannesburg, 1984. 16

, .

MALNUTRITION IN SOUTH AFRICA

'by Nonisa Ndaba and Chippy Olver SALDRU University of Cape Town

. , .

'. - f -, I 17

MALNUTRITION IN SOUTH AFRICA

South Africa has often been described as a dual economy; side by side with a well developed industrial, mining and agricultural economy there exist rural 'slums' - underdeveloped overcrowded homelands that are increasingly unable to support their populations. The nutritional status of South Africans parallels this dichotomy. On the one hand we have the typical 'western' picture of obesity, ischaemic heart disease and hypertension ieaching almost epidemic proportions amongst the affluent classes. On the other had is malnutrition, and a host of poverty related diseases. Nutrition is the central mediating factor between impoverishment, disease,

debility and premature death ~ this is the price that is paid by so many children today throughout the underdeveloped 'third' world.

PROTEIN ENERGY MALNUTRITION

(PEM) is the generally accepted term for the widespread malnutrition affect- ing primarily young children i,n developing countries. It is best considered as a spectrum of diseases resulting from variable·inadequacy of protein and calories as well as other nutrients, e.g. Vitamin A, Iron and calcium. Severe forms of PEM manifest clinically as marasmus and Kwashiorkor; subclinical forms are characterised by growth and developmental retardation. The conditions are further commonly complicated by life threatening infections.

PEM can be defined quite simply in terms of weight, and the presence or absence of oedema (i.e. pathological swelling of the body, face and limbs due to low protein levels in the blood).

BETWEEN 60 - 80% OF EXPECTED LESS THAN 60% OF EXPECTED WEIGHT (AGE SPECIFIC) WEIGHT

NO OEDEMA MILD TO MODERATE PEM MARASMUS

EDEMA KWASHIORKOR MARASMIC-KWASHIORKOR

I 18

The word ·kwashiorkor comes from the Ga tribe of Accra, and refers to the sickness the oldest child gets when the next baby is born; this coincides with weaning from the protein-rich breast milk diet.

Kwashiorkor is considered to arise from·a relative deficiency of protein in the diet, whereas Marasmus is due to an absolJJte de.ficiency of energy intake.

CLINICAL F~TU~ES OF KWASHIORKOR

The diseilse is characterised by failure to thrive, weight loss and eventually oedema, which masks the wasting and is obvi~us in the face and legs. It is when the oedema subsides that the trtie prictureof wasting becomes obvious. There is dermatosis resembling flaky paint, usually on the legs and buttocks. Hair changes are characterised by loss of curl and pigmentation in Negro children, so that the hair looks reddish-brown and is easily plucked. There is persistent diarrhoea, with food excreted almost unchanged, due to reduction in the amounts of absorptive enzymes. The problem is compounded by loss of appetite. making these children very difficult to feed.

BIRTH ---~) BREAST FEEDING 1 - 2 YRS ---')') WEANING 1 KWASHIORKOR ~(:--- ACUTE INFECTION ~(--- STARCHY WEANING FOOD

CLINCIAL FEATURES OF MARASMUS

Growth retardation occurs with wasting of subcutaneous fat and muscle; weight being a better index than skeletal· measurements such as length, and head circumference. 'The infant is often brighte~ed, alert and 19

hungry with a "wizened monkey" face. Gastro enteritis often occurs repeatedly.

The typical sequence of events may be summarised thus:

Breast-feeding ~ Early abrupt -----~> Use of overdilute, up to 5/12 weaning contaminated formulae

MARASMIC

But these clinical· cases, although prevalent throughout the third world, do not give us an accurate picture of the extend of undernutrition. The analogy of an iceberg has frequently been usedI,2,"3··with the clinical I cases of PEM representing only 3% of all undernourished children. . Further, subclinical PEM, that is the mild to moderate forms of under­ nutrition, affects between 60 and 70% of all preschool children within I the third world. .

THE ICEBERG OF UNDERNUTRITION

Recognised severe forms (3%) THE UNSEEN BURDEN .:. 60 - 70% of pre- Unrecognised mild to moderate (chronic in most cases) ~OOI childm undernutrition.

------~~--~~------~------20

In the face of this problem, most authorities consider anthropometric measures of undernutrition to be most useful in assessing this 'iceberg'.

The commonly used anthropometric parameters are age-specific height and weight measuremen't's; height-specific weight measurements, tricipital skin fold thickness, uppe'r arm, head and chest circuinstances. These para­ meters can then be compared with standard distributions for well-nourished children, and inferences then made as to as individual's nutritional status.

Well kept growth charts for children are thus of considerable value, as any deviation from .centile lines is easily 'recognised, and is a clear indication of nutritional deprivation and/or illness. The growth charts are derived from studies on North American children, the Boston and NCHS standards being commonly used. The 3rd percentile (80% expected weight) is taken as a .cut:off point, below which one would expect to find only 3% of children in any normal well-fed population.

Unless a child has regular measurements taken at a clinic, it is impossible to tell from any single study whether he/she is growing along centile lines, but one can place the child's measurements in terms of the normal distribution. This is obviously an inferior assessment, but in· the majority of third-world situations it must suffice.

, ' HiSh Risk Groups

Most of the preceding discussion has focussed on PEM during childhood. This is the most severely afflicted age group and also the most vulnerable. as the period between weaning off the breast artd the age of five is considered to be crucial. Not only is the child quite unable to look after its own needs at this time, it is also a period of rapid growth and consequently higher nutritional requirements per kilogram body weight than in adult life. Further, the children under 5 years of age are particularly 21

susceptible to.~iarrhoea, intestinal parasites, typical childhood diseases such as measles, and tuberculosis.

PEM is however also prevalent amongst scho~l-going children. A number of studies in South Africa indeed indicate that PEM amy well be more common amongst school children than their pre-school counterparts.

Pregnant mothers are also at risk, because of their obviously increased nutritional needs. Undernutrition influences their childs' birth-

"eight and lead s to increased per1nata' 1 morta l'1ty. 2. Even women wh 0

"ere malnourished as children tend to have smal1~r babies.

The elderly are an often ignored risk group. It is thus people at the extremes of life, who are unable to. work and earn a living that are affected. To this we can add another high risk group - the unemployed.

THE EXTENT OF MALNUTRITION IN SOUTH AFRICA

In 1968 Kwashiorkor ceased to be notifiable disease in South Africa. Thus the last available official statistics on Kwashiorkor. are for 1968 and are as fol1ows :

Whites 7 cases Coloureds 1046 Cases Asians 12 Cases Africans 9765 Cases quoted in 'Critical Hea1th,4.

This is clearly an underestimate, and a survey of 20 000 children carried out by the Department of Health and Welfare in 19802. revealed that approx­ imately 36% of coloured, 44% of asian, 27% of black and' 5% of white children between the ages of 6 and 9 years fell below the Boston 3rd percentile. 22

A survey of black children under 7 years of age in the Transvaal (1973) found 47,3% (rural) and 40,3% (urban) to be below the 3rd percentile for weight. 5 •

In 1977 a survey of Sowetochildren showed the following results.5•

Age (yrs) % below 3rd I!ercentile % below 3rd I!ercentile for weight for height

Under 2 18,9 63,S 2 - 5 29,1 66,4 6 - 9 38,9 55,S ;' 10 - 12 45,4 59,2 13 - 16 38,3 45,7

A recently compiled survey of the available data on malnutrition by T. Vergani2• gives a conservative estimate of approximately 2.9 million children below 15 yeras of age in South Africa (incliding the "Homelands") being below the NCHS 3rd percentile and showing signs of malnutrition. Of these, 1,5 million are reckoned to fall below 75% of the NCHS norms, and thus to have second degree malnutrition. Regardless of the standards used, PEM poses a severe problem for South Africa, especially within rural areas of the homelands, the resettlement camps ( particularly the Ciskei) and periurban squatter and townships communities.

The malnourished child has a supressed immune response, hence has increased susceptibility to infection~ Common infections such as measles, gastro­ enteritis and tuberculosis are immediately life-threatening. Conversely, infection is also a major cause of malnutrition and c,lassically a vicious cycle takes place:

POOR «MALNUTRI,ON SOCIO-ECONOMIC J ENVIRONMENT INFECTION 'I 23 I

Diarrhoea illustrates this case very well. Infants recently weaned off the breast often suffer recurrent episodes of 'weanling diarrhoea'. Malabsorption of dietary intake and dehydration precipitateS large losses of water and electrolytes and death can occur within hours. Death- amongst malnourished children is mostly due to water and electrolyte imbalances following diarrhoea and/or acute ,bronchopneumonia.

MALNUTRITION AND INTELLECTUAL DEVELOPMENT

An 11 year study using cross-matched children has shown a marked associat­ ion between severe PEM in early childhood, and later intelligence scores, 6 educational placement and motivation. • Further, a hungry child finds concentration in class difficult. Considering the so~ial background in which this occurs, and the poor standard of education offered t·o most black children, anyway, we may indeed agree with Dr Trudy Thomas when she writes: "If you set out deliberately, for the sake of behavioural ,I science, to produce a vicious and brutish person, you could hardly pick i a better set of deprivations.,,7.

INTERVENTION I I Immediate !

1. Rehydration dehydration is the biggest killer of children, 'and is easily treated with a solution of salts and sugar, given orally.

1. Food intake is begun cautiously and increased slowly' - the child's gut and dig~stive enzymes are invariably damaged i~ severe PEM, and must recover. Milk and oil mixed in with the staple diet are'frequently used.

3. InfectiOns, anaemia and vitamin deficiencies must be cured. 2.4

In the Community

l~ Provision of clean water, to minimize the risk of infection.

2. PromotiOn of breast-feeding - not only is this of inestimable benefit to the child but it also serves as a n~tural c0ritracePt~ve.

3. Immunization, to reduce infections.

4. Growth monoto·ring, to detect early cases.

5. Family planning.

6. Accessible clinics and nutrition day-care centres.

7. School feeding schemes

Medium-term

Proposals have been made'to tackle the problem from a deeper- perspective. These include:

1. r,ura!- de~elopment p.rogrammes, with emphasis on appropriate technology for agriculture.

2. self-help schemes.

3. alterations in government food policy.

4. food subsidization.

5. mobilization of the business sector.

These suggestions are unlikely to be heeded by those who control the required resources. Even so, they do not tackle the roots of the nutrition problem. Food is a social necessity. Its use as a means of profit demonstrates the blatantly ignorant and/or callous attitudes of the controllers of agriculture and food distribution. Long term solutions must seek to alter that control, such that the social function of food becomes

I 2S

paramount in determining its destribution, and this implies fundamental

~hanges in the system of land ownership.

"THE LAND SHALL BE SHARED AMONG THOSE WHO WORK IT!

Restrictions of land ownership on a racial basis shall be ended, and all the land redivided amongst those who work it, to banish famine and land hunger;

The state shall help the peasants with implements, seed, tractors and dams to save the soil and assist the tillers;

Freedom of movement shall be granted to all who work on the land;

All shall have the right to occupy land wherever they choose;

People shall not be robbed of their cattle, and forced labour and farm prisons shall be abolished."

extract from the Freedom Charter, adopted at Kliptown, 1955. 26

REFERENCES l. Malnutrition and Apartheid - N. Anderson, 1978; prepared for the Food and Agricultural Organization of the U.N. FFHC/Action for Development Bulletin, Special Issue on Southern Africa.

2. Malnutrition in South Africa - T. Vergnani, February 1983; publ. by Unit for Futures Research, University of Stellenbosch.

3. Nutrition for Developing Countries - M. King, F. King, D. Morely, L. Burgess, 1976; publ. by Oxford University Press, Nairobi, Kenya.

4. Food - For People Not for Profit - Critical Health No.6, November 1981.

5. The Problem of Malnutrition in South Africa - Y. Rechav, publ. in SAMJ June 13, 1981.

6. Protein-Calorie Malnutrition in Children and Its Relationship to Psychological Development and Behaviour - M.C. Latham, publ. in Physiological Review, Vol. 5L, No. 3 July 1974.

7. Their Doctor Speaks - Trudy Thomas, 1973; publ. by Mary Wheelden. 27

TUBERCULOSIS

by Chippy Olver SALDRU, University of Cape Town 28

TUBERCULOSIS

70 - 80% of all notified diseases in South Africa are due to tuberculosis. 1• It is thus the most prevalent arid publicly hazardous disease amongst" the poor here today, claiming between 6 and '10 Iives daily 2. and being responsible for over 6% of all de"aths amongst" black Africans.3•

Of all TB" cases, 80% are black, 15% 'coloured', 1,5% Asian, and 1% 'white'. Tuberculosis is particularly prevalent in the "homelands", the worst affected areas in South Africa being the Transkei, and Ciskei, "and the coastal belt down to Port Elizabeth, as can be seen below.

%oFTllEPOPULATlOO WITH OPEN P\JIM:I'lARY (INFFX:TlOOS) TB

o 10 20 30 40 50 60

Zululand "I II I I I II

Transkei I I I I I I I I I I I I I I I II I I I I I I I I I I I I I 1"1 I I I I I I I I I I I I I I I I I I I I I I I I I I I I I

Ciskei "'" II " II II II " II II II Gcizankulu +I- Lebc:wa + Bophuthatswana II I I I II I I I I

Source TBRI surveys, as quoted in (5).

Pathogenesis and Clinical Features

Two factors are essential for the development of the;disease.

1) infection with the bacteria Mycobacterium tuberculosis, alternatively Mycobacterium bovis.

2) a receptive individual, whose bodily defences have been worn down by physical and mental stresses. 29

Both factors are intimately linked with basic living_and working conditions and hence socio-economic status, making TB the classic disease of poverty.

Important elements include poor nutrition, physical and emotional stress,

long hours of hard labour in poor working condition~, constant exposure to TB bacteria, old age, alcoholism, and a variety of disease states.

Its transmission is facilitated by crowd~d conditions, and certain working environments (e.g. mining). It thus occurs predominantly amongst the working class and peasantry.

Three age groups are primarily affected. Initial contact generally occurs in the young child who~e immune system is immature and who frequently suffers from malnutrition. A primary infection usually develops in the lung and this may spread elsewhere in the body. 85% of cases recover completely and remain immune to TB, while 15% retain bacteria in the scar tissue and the disease becomes latent. There are thought to be between 5.5 and 7 million cases of 'latent' TB in South Africa today.2.

In later life the disease is usually a manifestation of reactivation of latent infection. Prime candidates for this are people, in their 20's and 30's (men more often than women), worn out by work and inadequate diets, who are trying to raise a family in an impoverished environment. The other major group js thf, eld'erly who are unable to support themselves, either with or without pensions, and forced to rely upon the extended family for their survival.

The disease is now far more destructive, and gives rise to the well known picture of active pulmonary TB, with chronic cavitating infections, scarring and tissue destruction. Without correct treatment over 60% of affected patients will die.

The symptoms include a persistent cough productive of foul-smelling sputum and occasionally blood, weight-loss leading to emaciation 30 a continual lack of energy, and intense sweating at night. Gradually the symptoms worsen. These cases are highly infectious. Some 45 000 are notified annually in South Africa, but the true number 2 possibly is closer to between 70 and 100000 cases. • A frightening number of TB sufferers remain undetected, and untreated.

FIG. 2 INFECTIOUS POOL OF TUBERCULOSIS

__------__ ~------==:>6 - 10 deaths daily in South Africa

2,2% annual risk of amongst blacks

reac.tivation primary TB reinfection childhood

5,5 - 7 million cases of latent TB in SA. 85% recovery 31

FIG. 3

NEW CASES OF TB PER ANNUM, PER 100 000 POPULATION

Transkei + Ciskei 490 Other 'independent' homelands 370 'Whites'/Indians 30 RSA 'Coloureds' 260 Urban blacks 190

Source H. H. Kleeberg SAMJ 17. "1.82 (1980 Estimate)

Ttle Roots of the Problem

At the beginning of the last century TB was virtually unheard of in South Africa. The TB epidemic has developed over the la"st 150 years. Its syread throughout the rural areas. of South Africa has paralleled·the development of the mining industry and the migrant labour system. it was on the mines that African labourers first encountered the disease, carried from the ! north by European miners. Long hours spent underground working in humid and dusty environments, coupled with low wages, inadequate diets and frequently complicated by other ~ccupational lung diseases, such as s iii cosi s, created the perf~ct condi tio~s for. the. di sease_: Mi gr~nt workers who contracted TB were immediately sent back to their homelands, inevitably infecting all those around them.

The rural subsistence econqmies were in the process of collapse, hastened along by a series of taxes and land acts. Unemployment and low wages had brought these populati.ons to the brink of starvation. an excellent breeding ground for the tuberculosis bacteria. By 1860 TB was already rife amongst blacks in the Transkei and Cape province and the situation prompted a number of commissions of inquiry. In 1883 the Cape Public Health Act was, 32

passed, giving special attention to the TB problem. The Native Mine Labourers Commission was appointed in 1911, and the Tuberculosis Commission in 1914. Despite these efforts, by 1930 72% of blacks recruited for mi ni ng had evi dence of previousi nfecti on wi th T B. 5. The 1932 Tuberculosi s Research Committees Report gave the following alarming statistics for the Ciskei f.IG. 4

2 23; Tests were donei n Rural Vi Ilages in the Ci skei: 1. children under 5 years yielded 37% positive reactions. 2. children 5-10 years yielded 60% positive reactions. 3. children 10-15 years yielded 71% positive reactions. 4. persons 15-20 years yielded 81% positive reactions. 5. persons 20-25 years yielded 93% positive reactions. 6. adults over 25 yeras yielded 90% positive reactions.

The incidence of TB amongst blacks climbed steadily during the 1930's and 40's following the growth of industrializat'ion and overcrowded peri-urban settlements. Amongst 'whites', however, the TB rate had started to fall. This was largely due to their improved socio-economic status following the state's efforts to solve the 'poor white' problem.

New Hope?

Then in the late 1940's the first drugs that effectively treated TB became available. The department of health, in conjunction with local authorities and SANTA, instituted active case finding using mass X-ray screening tech­ niques and tuberculin skin tests. As a result the number of notified TB cases surged, levelled off during the 1960's, and started to fall dramatically during the 1970's, (partly due to the exclusion of the Transkei statistics from those for the rest of South Africa). Nevertheless it is generally 33 accepted that the notification rate gives a highly inaccurate picture of the TB situation. A far more sensitive indicator that is used is the annual risk of infection with TB amongst children, expressed as a percentage. Medical Research Council surveys have used this indicator to show the following improvements in the TB situation over the last 20 years.

Annual risk of infection with TB amongst children - improvement over 20 years

'Whites' 1,5% to 0,1% (93% reduction) 'Coloureds' 3,9% to 0,6% (75% reduction) Asians 2,2% to 0,4% (59& reduction) Blacks 5,0% to 2,2% (56% reduction) Source: Glathaar SAMS. 17.11.82

Nevertheless, the MRC surveys showed an excessively high risk of infection for certain areas :

FIG. 6

Annual risk of infection with TB amongst black children (1974-77)

Transkei 4,5% Ciskei 4,5% Port El i zabeth 3,5% East London 3,0% Kimberley 2,0% Source : MRC surveys, as quoted in 6.

As pointed out in 6. the main evidence for the improvements noted above comes from the urban areas. The TB epidemic in the rural areas remains, and it is perpetuated by three major f~ctors 1. the landlessness of the Transkei and Ciskei peasants, who must rely on the meagre wage packed of migrants. The manager of Wenela recruiting organisation for the Chamber of Mines has said: 34

,'Our wage isn't sufficient to meet the needs of a man and his family, unless it is augmented by'earnings from a plot of land in the man'S homeland. A family man from Johannesburg, for instance, couldn't live on what we, pay.'

2. the inadequacy of rural health se~vices, especially those for long term TB treatment. Th'~" South African Department of Health ,no longer accepts any' responsiblity for the treatment of TB in the' 'independent' states. •

3. the" policy of repatriating miners infected with TB. Up until a few years ago at least 1 '000 Transkeian miners were repatriated annually after' a limited courSe of treatment.6•

4. non-compliance in the treatment for TB takes many months; without adequate supervision, and a careful explanation by'tbe doctor of the p~rpose of ,thi s course of treatment, the TB pati ent wi 11 stop taki ng hi s medication¥as soon as he feels better.

TB Control

. At the'National Tuberculosis Conference held in 1979 in Pretoria, a control programme was adopted, the aims of which ~ere to reduce.t~e annual risk of infection with TB U0';O,3%, and to provide effective treatment for all TB sufferers. The main elements of this programme are:

1. Involving the community in education about rB.

2. Supervised short-course treatment for TB cases. There are oniy 11 600 hospital beds available for TB patients, and the intention is to provide ambulatory care for most cases. ~sing 4 anti-TB drugs (including Rifampicin) it is now possible (and cheaper!) to treat patients in 4-6 months, instead of the 12 month treatment without Rifampicin. 2.

3. Active case finding, to reduce th~ number of inflectious TB cases;

4. Innoculation with the BCG vaccine. Three doses of vaccine are required for effective protection from TB; in 1973 BCG vaccination 3S

was made compulsory. and it was decided to vaccinate all 1) new borns 2) 3 month old infants 3) school beginners 4) school leavers

Due to the budgetary restrictions this programme has not been fully implemented. In 1982 the TB budget was R43 million. E. Glathaar2. estimates that an i ncreas_e to R59 mi 11 i on per annum by the end of 1984 wi 11 be reQui red to implement the control programme effectively. He then anticipates that this amount'will fall steadily after 1986. as the TB rate drops.

CONCLUSION

While the above proposals are certainly called for. they fail to attach sufficient importance to the socio-economic mileau within which'TB occurs. The low incidence of TB in the urban areas is due first'ly to the improved standards of living of urban populations. and: only secondly to the TB services available there. Individuals who are cured of TB are returned to the same- impoverished conditions that-generated the disease' in the first place; this accounts for the high relapse rate. At present 38" of all ,TB patients in hospital are relapse cases.2• Studies of TB in the developed countries of the West show that the incidence of TB had been falling dramatically for many years PRIOR to the introduction of anti--TB drugs and BCG vaccination. These improvements matched the improving life styles of the working class in these ,countries. Without doubt such improvements are the treatment of choice for TB. Better housing. adequate ,wages. improved working conditions. the abolition of migrant labour, and an equitable distribution of land in the rural areas are fundamental pre­ requisites for any TB controlprogramme.OsJ:.or~ stated back in 1945: 'Poverty causes tuberculosis - we should make it our business to understand tpe cause of that poverty and to dissipate that poverty. '( - - 7) 36

REFERENCES

'Consumption in the Land of Plenty - TB in South Africa - a collection of papers at the uct Medical Students Conference on TB, 2nd-4th August 1982, publ. by Medical Students Council (UCT), - this is an excellent exposition of the TB situation.

1. Monthly notifications of diseases, published in the South African Medical Journal.

2. 'Tuberculosis control in South Afric~, 'Where 'have we gone wrong?' and 'A look at the future' - E. Glatthaar, SAMJ special issue, 17 November 1982.

3. Report on Deaths of Blacks in Selected Magisterial Districts, 1977. '

4. The dynamics of tuberculosis in South Africa and the impact of the control programme - H.H. Kleeberg, SAMJ special issue, 17 November 1982.

5. Tuberculosis in South Africa - N. MacVicar, 1932 pubi., in Outlook on a Century. 1870-1970. F. Wilson and D. Perrot (eds.), Lovedale. 1972.

6. Tuberculosis in.South Africa in the 1970's - N. Whit~, publ. by Health Care Trust. 17 Main Road. Mowbray.

7. Socio-economic aspects of tuberculosis - T.W.B. Osborn. Physiology Department. Wits, publ. in The Leech. August, 1945. 37

DIARRHOEAL DISEASE IN YOUNG CHILDREN

by Anton van der Merwe Fifth year Medical Student, UCT. 38

DIARRHOEAL DISEASE IN YOUNG CHILDREN

DESCRIPTION AND CAUSES

The term "diarrhoea" means the passing of excessive numbers of loose stools. This is often accompanied,by vomiting and together these two 'factors'result in an excessive loss of water and electrolytes (salts) from the body; It is almost always caused by a Viral, bacterial o'r parasitic infection but it is usually not possible to tell which organism is responsible (indeed two or. more. may act 'together). This is not particularly important however since 'the treatment is basi,cally the same irrespective of the cause.

Diarrhoea is very common amongst small children in all countries and amongst all socia-economic groups. Studies, have shown that on average a child can be expected to suffer from 1-12 episodes of diarrhoea per , year, 1,2.,

The following factors, however, are accociated with firstly an increased incidence of attacks; secondly an increased severity of individual attacks; thirdly an increased mortality from the attacks and fourthly a protracted', recovery time from episodes of diarrhoea:

1. lower social class 2. poor sanitation 3. decreased availability of clean water

4. malnutrition

5. bottle feeding rather than breastfeeding.

In addition, the ignorance of the best simple remedy for the disease and poor health facilities are associated with an increased severity and mortality. 39 2

These factors account for the paradoxical fact that whilst diarrhoea is one of the commonest minor illness's of childhood it is also one of the main killers of children ( up to 60% of deaths in parts of In,dia and South East Asia, unfortunately no accurate figures are available for RSA).

Diarrhoea is a minor illness when it occurs in a healthy, wellnourished child and is treated early and appropriately. It is a dangerous disease in malnourished children especially when treated inappropriatly. Diarrhoea

not only kills directly, however; it is a major ~ of malnutrition and frequently precipitates the development of kwashiorkor/mara~mus in a child who was just coping previously. And these malnourished children are also at a greatly increased risk of dying from other infectious diseases (e.g. TB and measles).

NECHANISM

The way in which infections cause diarrhoea is not entirely understood but 2 main mechanisms have been identified:

1. the production of a toxin which stimulates the secretion of electrolytes (salts) and fluids by the cells lining the gut.

2. damage to the gut wall resulting in poor absorption as well as leakage of fluid and electrolytes.

COURSE OF THE ILLNESS

The main features of the illness are:

1. the sudden onset of diarrhoea which is usually watery but may be thicker and varies in colour. There may be blood in the stools.

2. vomiting, which may begin before or after the diarrhoea.

3. dehydration, (sunken eyes, dry mouth and tongue, drowsiness, jitteriness, cold hands and legs, and a fast pulse rate). 40 3

In severe, untreated diarrhoea, shock, fits and eventually coma and death will occur.

TREATMENT

The single most important con'cept in treating diarrhoea is that the children are losing water and electrolytes (salts) and these must be replaced as early as possible after the diarrhoea begins with a mixture of water, salts (mainly sodium, potassium and chloride) or sugar (glucose or sucrose). This is most simply and effectively given as a drink by mouth. Meals may be vomited out again and lost in the stools but this is not important, the aim is to give more than is lost. Normally 20Oml/kg body weight/day will suffice. Only in fairly advanced cases will a nasograstric tube or an intravenous line be needed for fluid administrat­ ion. It is usually recommended that milk feeds should be stopped for no more than 12 - 24 hours and that full strength breast or cows milk feeds should begin thereafter (Ransome et al)~· With this treatment the diarrhoea usually resolves within a few days. Antidiarrhceal QTUP.S should never be used and antibiotics are rarely needed.

The discovery that water, salts and sugar must be given to replace fluid and salt loss (since sugar is needed for salt absorption)' was made as recently as the late sixties. This was a major advance in medicine and reduced the mortality from cholera to less than 1% of serious infection. Unfortunately this advance irr knowledge has not been coupled with effective dissemination, understanding and application of the knowledge. Mothers often believe (understandably) that the best way to treat diarrhoea is to withhold fluid, with. disastrous consequences.

Major efforts have been made, with some success, to teach mothers the simple principles of treating diarrhoea. And simple guidlines to mix salt, sugar and water have. been drawn up. 41 4

One of the simplest regimen is:

3.5 grams of table salt (about 8 pinches with 2 fingers and one thumb.)

.30 grams of sugar (one four finger scoop)

.1 litre of water (boiled preferably)

. mixed and given by mouth

Although not ideal, the advantage of this regimen is that it can be llsed by just about any mother under just about any circumstances.

A more scientific reginen is:

.Sodium chloride (table salt) 3.5 grams

.Sodium bicarbonate 2.5 grams

.Potassium chloride 1.5 grams

.Glucose 20 grams

.1 litre of boiled water

.Mix and give by mouth

DISCUSSION

Diarrhoea is one of the few important causes of increased morbidity and mortality amongst poor people that can be treated cheaply and effectively without major socio-economic advances. For this reason it is difficult to accept that there is still such a high mortality and morbidity from this common disease. 5 42

REFERENCES

1. J.E. Rokde and R.S. Northrup. Taking science where diarrhoea is. In - Acute Diarrhoea in Childhood, CIBA foundation symposium No. 42, p. 339 - 366.

2. J.E. Rohde and L. Hendrata. Oral rehydration: technology and implementation. In: Advances in international maternal and child health, Vol. 1. Jelliffe and Je1iffe (Eds.) Oxford Medican Publications ·(1981).

3. D.J. Ransome, Herna Roode. Early introduction of milk feeds in accute infantile gastroenteritis. South African Medical Journal 64:127-128 (1984).

FURTHER READING

Acute Diarrhoea in Childhood. Ciba foundation symposium No. 42 (1976).

M.D. Bowie and I.D. Hill. Acute infectious diarrhoea of childhood gastroenteritis. In: The South African Journal of Continuing Medical Education. January 1983.

G.J. Ebrahim. Pediatric practise in developing countries. MacMillan Press Ltd. (1981). 43

by Anton van der Merwe 5th year Medical Student, UCT. 44

CHOLERA

DESCRIPTION AND CAUSES

Cholera is an infectious disease characterized by the sudden onset of diarrhoea and vomiting of varying severity lasting for 1 to 5 days. It is caused by vibria cholerae, a bacteria which is passed in large numbers in the stools of infected patients. Drinking water and food is contaminated by these stools and results in the spread of the disease.

The "EI tor" biotype of vibria cholera, which is responsible for the current pandemic (world wide epidemic) is different from the other "classical".biotype because for every 100 infected (and therefore infectious) cases only about 2 will have obvious diarrhoea. The other 98 although unaware of their infection, will nevertheless spread the disease wherever they defaecate. Thus the disease spreads viciously and quickly.

This fact, and the fact that it can kill so rapidy(often within one day) make cholera ·one of the most formidable and difficult to manage infectious diseases.

From the time of the pandemic of the mid-19th century South Africa was relatively free from cholera until the current epidemic began in October 1980 in the Malelane area of the eastern Transvaal.

This epidemic is really an extension of the current seventh world wide pandemic and was anticipated by South African health officials as early as 1973. Increased surveillance and hasty attempts to control spread were, however, unable to prevent the rapid spread of cholera into the Transvaal, OFS and down the east coast. 45 2

As can be predicted by the nature of the disease, cases of cholera occur predominently :

I) in areas where there is no supply of clean water "

2) in areas where sanitation is poor and

3) in areas where there is overcrowding.

In addition it is not surprising that more deaths from cholera occur ,·:here health facilities are deficient.

Because about 100000 patients with overt cholera'have been treated since 1980 it can be ,eiltimated that about 2-3 million cases of cholera infection have occurrred. Most of these have been in KwaZulu, the Transkei and Ciskei.

it seems that cholera is now becoming endemic in South Africa i.e. present throughout the year although the prevalence increases in the warm, wet summer months. Evidence from other epidemics' suggest that the age distribution of cases will change from affecting predominantly adults (as it is nOl" ) tC) involving more children. Cholera is however rare in children under one year old.

MECHANISM OF THE DISEASE

The cholera bacteria, after ingestion, mUltiply and attach to the lining of the small intestine. They secrete a toxin which binds to the cells and results in a rapid outpouring of fluid ~nd electrolytes (salts). It is this 'loss of fluid and electrolytes that causes all the symptoms and kills'the patients.

COlJRSF OF THE ILLNESS

The main features begin about 1 to' 5 days (less in children) after the person is infected. •

46

3

The consist of the sudden onset of : 1) diarrhoea: which varies in severity from mild to massive (up to 20 litres per day). The stools are watery and amy be green, yellow or like rice-water in appearance. 2) vomiting: which is usually effortless

3) cramps: these occur later on, can be severe, and affect mainly the abdomen and limbs. They are due to dehydration and resolve rapidly with treatment.

Untreated patients rapidly develop:

4) dehydration: seen mainly as thirst, sunken eyes, dry mouth, loss of weight, and 5) shock: seen as low blood pressure, rapid pulse and cold hands and feet.

The temperature is usually normal or low and the patients are usually alert children differ in that they frequently become drowsy, amy have fits and often hav~ a fever.

TREA1MENT AND ourCCME

The mainstay of treatment is the early administration of water, salts and sugar in large quantities to the patient.

It is usually possible to give these by mouth, the simple principle being to give them faster than they are lost through the vomiting and diarrhoea. The intravenous route may be needed in. severe cases or where vomiting is profuse. On average about 15 litres of fluids will be needed, often far more.

i 4 47

..I recommended regimen is:

.3.5g of sodium chloride (table salt) .2.5 of sodium bicarbonate .1.5g of potassium chloride .20g of glucose . mixed in 1 litre of water (boiled)

In an emergency ~he sodium bicarbonate and potassium chloride can be left out and ordinary sugar (sucrose) can be used instead of glucose. The most important point is that sugar and salt must be given in the water since they are obsorbed together from the intestine.

Tetra eve] inc - an antibiotic - is given routinely in a dose of 500mg every 6 hours for 5 days in adults. h'i th this treatment the patient recovers rapidly, often dramatically and the mortality from severe cholera is less than 1% (0,6% in KwaKulu).

PREVENTION

Short-term prevention

Accepting that a risk of infection exists and that water sanitation and health facilities are suboptimal, the following measures may prevent infection :

1) boiling or sterilizing with chlorine or hypochlorite, all water ingested or used in washing or preparing of foods

2) disposal of vomitus and stools well away from water supplies and food.

3) washing of hands before handling food and other defaecation.

4) washing of fresh fruit and 'vegetables before ingestion.

Mass immunizatianor mass chemotheraphy are very expensive and largely ineffective. r

48 5

Short-term Measures

These are for more important and are essential if epidemic cholera is to be eliminated.

Appropriate measures are:

1) supply of clear water - this is the single most important factor

2) adequate sanitation facilities

3) improved housing· and elimination of overcrowding and malnutrition

4) improved health facilities

CONCLUSION

It seems obvious from the above that cholera is a disease of poverty. Eliminate poverty and the disease will cease to exist. Indeed, the U.S.A. has had less than 2 dozen cases in the past 50 years. Great Britain has had less than 30 cases reported in the past 50 years.

Further Reading: 1. Cholera. In Pediatric practice in developing countries, p. 151. G.J. Ebrahim, MacMillan Press Ltd., 1981.

2. M.A. Seedat. Cholera in South Africa, Modern Medicine September 1982, p. 81.

3. M.A. Seedat. Epidemic Cholera in South Africa, South African Journal of Continuing Medical Education, Volume 1 No.1.2, p. 22. 49

SEXUALLY TRANSMITTED DISEASES

by Margie Duncan University of the Witwatersrand, Johannesburg so

The extent of the problem in South Africa

Although it is generally agreed that sexually transmitted diseases (STD) has assumed frightening proportions in S.A., both among the poor and the wealthy, cases are not notifiable by law and exact figures of incidence and prevalence are thus tmavailable. An index of numbers can be guaged however from the fact that 600 000 people attended municipal clinics in this country in 1983. This is obviously an underestimate as sufferers seek help from a variety of sources both within the private and public sector.

Pathogelnesis

Bu definition, sm is acquired by sexual contact with an infected partner. Promiscuity plays a major role in the spread of these infections and this may be aggravated by alcohol abuse, leading to loss of inhibitions and indulgence in casual sex. Casual sexual encounters are also a byproduct of this migrant labour system as men have to leave behind a stable relation­ ship to seek work in the urban situation. Common, yet less important STDs such as public lice and scabies, are aggravated by overcrowding and poor hygiene.

Clinical Picture

In men the commonest presenting feature in URETHRITIS, 1 "& 2 characterised by a discharge from the urethra, which may be accompanied by burning on passing urine and frequency. The organisms which most frequently cause this, namely Neisseria gonorrhoea and Chlamydia trachomatis, if not eradicated, may track further to cause an acutely painful, warm swelling within the scrotum (EPIDIDYMITIS)3 which could result in infertility later in life.

Unfortunately the female contacts of these patients rarely present with physical signs early on in the disease. Occasionally she will complain 51

of a vaginal discharge, but more often it is only when the infection has spread to involve the fallopian tubes (SALPINGITIS)4 that she presents for treatment with lower abdominal pain and burning when passing urine. Without treatment or with inadequate treatment, partial tubal blockage results, with its risk of ectopic pregnancy. Especially when recurrent episodes occur, complete tubal occlusion may result, with ensuing infertility.

An infected pregnant woman may give birth to a baby who suffers from con­ junctivitis (early, on, in gonococcal and about 10 days later, in chlamydial infections). Chlamydial infection may also lead to chest problems in the neonate.

Sexually aquired GENITAL ULCERATIONS 5,6,7. present another problem. The most important of these is SYPHILIS because of its long term co,plicat- ions, which may be fatal. Fortunately these are rarely seen today. Syphilitic ulcer, which are frequently painless are accompanied by painless swellings in the groins. They often pass unnoticed, especially in women. In both sexes ulcers disappear spontaneousaly and the patients may develop skin rashes or flat topped lesions in the moist regions (usually genital or around the anus), or the patient may be asymptomatic, yet carrying the infecting organism in the blood and secretions of the body, thereby unknowingly infecting sexual contacts. Syphilis in pregnancy may result in abortion, still-birth or a baby with congenital syphilis.

Also common are CHANCROID ulcers, characterised by soft, painful lesions with a dirty base and 'in about 50% of cases associated with a tender swelling in the groin.

There is an increasing incidence of HERPES GENITALIS, which presents as groups of blisters which rapidly break down to form superficial ulcers. There is often a history of recurrent episodes. Women with an active attack during labour run the risk of infecting the baby passing through the birth canal. There is also an association between. cancer of the 52

cervix and genital herpes sufferers.

The two other major sexually transmitted genital ulcers, namely LYMPHOGRANULOMA VENEREUM and GRANULOMA INGUINALE are largely restricted to tropical and subtropical areas of the Eastern Transvaal lowveld, Swaziland and adjoin- ing areas of Natal and Transkei.8 •

Many women suffer from sexually transmitted VAGINAL DISCHARGES. Excluding thos mentioned before, namely gonococcal and chlamydial, there are 3 major causes: candidiasis ·(thrush),9 •. trichomoniasislO and Gardnerella- associated vaginitis. II. Candida, giving rise to a thick, adherant, white discharge and trichomonas, where.the discharge tends to be frothy,yellow-green in colour and thin, may both lead to itching, excoriation, burning urine and even dyspareunia. Gardnerella- associated vaginitis is distinguished by its offensive, often 'fishy' odour, and is otherwise asymptomatic.

Another sexually transmitted infection, occuring frequently in both sexes is the viral or veneral wart (CONDYLOMA ACUMINATA). These start as small pointed projections which progress to form large cauliflower masses.

MANAGEMENT

When STD is suspected it is essential to refer the patient to a doctor or clinic as soon as possible in order that the correct treatment be instituted before the disease is spread furhter. Education of the community is

vital, pointing out the haza~ds of promiscuity and the complications which may occur. It is important to stress the importance of treating the sexual contacts at the same time; whether ·they are symptomatic or not •. The use of condoms should be encouraged as this affords some protection . against contracting these diseases. Pregnant women and all STD sufferers

s~ould have blood screening tests for syphilis. Women with a history of Herpes genitalis should be monitered carefully during pregnancy and should have 6 monthly Papanicolaou smears for the early detection of cancer •

.- 53

REFERENCES

1. Oriel, J.D. Urethritis and associated infections: aetiology, diagnosis and treatment. S Afr J Sex Trans Dis 1981:1:14-18.

2. Ballard, R.C., Fehler, H.G., Duncan, M.O., Van der Wat, I.J. Urethritis and associated infections in Johannesburg the role of Chlamydia traichomatis. S Afr J Sex Trans Dis 1981 1 : 24-26. 3. Harnisch, J.P., Berger R.E., Monda, G., Rolnes, K.K. Aetiology of acute epididymitis. Lancet, 1977 1 :819-221.

4. Westrom, L., Mardh, P.A. ,Epidemiology, etiology and prognosis of acute salpingitis a study of 1457 laparoscipally verified cases. In : Hobson, D. Holmes, K.K., eds. Nongonococcal Urethritis and Related Infections. Washington DC: 'American Society for Microbiology, 1977: 84-90.

5. Duncan, M.O., Bilgeri, Y.R., Fehler, H.G., Ballard, R.C. The diagnosis of sexually acquired genital ulcerations in Black patients in Johhannesburg. S Afr J Sex Trans Dis : 1981 : 1 : 20-23.

6. Crewe-Brown, H.H. Krige, F.K. , Davel, G.H., et al.Genital ulcerations in males at Ga-Rankuwa Hospital, Pretoria. S Afr Med J 1982 : 62 : 861-863.

7. Meheus, A. , van Dyck, E. , Ursi, J.P. , Ballard, R.C., Piot, P. Etiology of genital ulcerations in Swaziland. Sex Trans Dis 1983 : 10 : 33-35.

8. Ballard, R.C., Duncan, M.O. Problems in the management of sexually transmitted diseases in South Africa. S, Afr Med J. 1983 : 64 : 1083-1086. 54

9. Young, C.N. Candidal Vaginitis. S Afr J Sex Tans Dis 1982 2 : 30-33.

10. Ross, S.M. Trichomonas vaginalis - a Review S Afr J Sex Trans Dis: 1982 : 2 : 2-6.

11. Piot, P., van Dyck, E. The pathogenesis and management of Gardnerella­ associated vaginitis: S Afr J Sex Trans Dis, 1981 1 : 2-3. ss

POLIOMYELITIS

by PETER DISLER Department of Community Health, UCT 56 POLIOMYELITIS

DEFINITION

Poliomyelitis (polio) or infantile paralysis is an acute infectious disease of the motor nuclei of the spinal cord and brain stem. It can be caused by anyone of three different strains of the polio enterovirus which enters the body via the nasopharynx and intestinal tract. As it is nowadays a totally preventable disease, its occurrence in any country is an indictment of the health services.

CLINICAL FEATURES

The majority of patients who are infected by the virusHTeeitherasymptomotic or suffer from a mild general infection. In the early phases this includes the nonspecific features of fever, headache, sore throat and gastroenteritic disturbances which may progress to increasing headache, pain in the muscles and delirium. Most patients recover from this illenss with no harmful effects ; in the minority it heralds the significant problem of paralysis.

The Paralytic Stage

The paralysis is asymmetrical and patchy but may be wide spread. The lower limbs are effected more than the upper and a serious manifestation is involvement of the intercostal muscles and diaphragm which can seriously embarrass respiration. The brain stem may be affected with consequent impairment of cranial nerve function and paralysis of the facial muscles I and those responsible for swallowing. -This is said to be rare in Blacks. .

Prognosis

The mortality in the paralytic phase may be as high as 25%2. and usually results from respiratory paralysis. The availability of sophisticated respiratory support equipment will thus markedly influence the mortality rate. S7 2

Not all muscles which are initally paralysed remain permanently impaired. Improvement usually begins at the end of the first week after paralysis first appears and may continue for at least a year. Permanently paralysed muscles will atrophy and the growth of the affected limb is often retarded.

Epidemiology

In the days before the vaccine was developed it was said that paradoxically members of developing communities, impoverished and with poor sanitation and overcrowding, acquired the virus earlier in life and presented in the main with nonparalytic or asymptomatic disease. Paralysis was thus the affliction of the less poor and well developed communities.' The widespread availability of vaccine has changed this situation and it is now a rarity in communities where vaccination cover is meticulous.

As it is a notifiable disease (i.e. all cases must be reported by law to the authorities) an index of the efficiency of vaccination in controlling polio in South Africa can be seen from the following figure.3. 3 58

There is no doubt tl>at the total incidence has decreased. However, the disease has now become the province of those who have limited access to health services. That the problem still exists is demonstrated by the 1982 epidemic of polio in Gazankulu3. In May 1982 the first child was admitted to Letaba hospital with paralysis. In the.next '2 months a total of 153 cases were admitted in the area, the incidence in the worst affected 1 - 3 year age group being close to 3 per 1000 pODulation. ',The vaccination status of ,the ,affected children provides

some insight i~to the causes of this epidemic :'.61,4% of the sufferers had no immunization, 19,6% did not lmow and, many of .the others had not received .the requisite 3 doses of vaccine. In the Retavi district of Gazankulu the overall vaccination rate ,was said to be'cI'ose 'to 50% although the inaccuracy of popUlation estimates may render this figure even lower. This tragic outbreak was thus largely preventable at

relatively low cost. l ~: ;

MANAGEMENT OF POLIO Primary Prevention

By law, all children in South Africa should receive 3 doses of the oral vaccine (Le. the 3 strains) at the age of 3, 4 ! and 6 months. The vaccine is highly effective, easy to administer and relatively cheap.

Management of Official Cases The therapy is largely supportive but care must be taken to avoid loss of patients through respiratory paralysis or aspiration of secretions in the presence of bulbar paralysis. Transfer of such a patient to a relatively sophisticated centre is probably mandatory.

Rehabilitation

Early attention must be paid to the physiotherapy to prevent contracttires. The management of the already paralysed individual follows the lines described in the chapter on disability. 59

4

REFERENCES

1. Clinical medicine and health in developing Africa. eds G.D. Campbell. Y.K. Seedat and G. Daynes. Cape Town : Tlavid Philiu Publishers. 1982

2. Brain's Clinical Neurolo!!y. Roger llannister. London Oxford University Press.

3. Epidemiological cOlJlllents. Vol 9 No 7 • .1ulv 1982. 11eoaTtment of Health Welfare and Pensions. Pretoria. 60

RHEUMATIC FEVER

by Peter Bundred, Hout Bay, Cape. 61

DEFINITION

Acute Rheumatic fever is a systematic febrile illness which is a sequal to a Group A beta-haemolytic streptococcal infection of the nasopharynx in a specifically suceptable host. The only long-term complication is rheumatic heart disease which occurs as a result of scarring and distortion of the heart valves by the rheumatic process.

ETIOLOGY

Rheumatic fever results from an interraction between the agent, the human host and the environment.

The agent is the Group A beta-haemolytic streptocuccus which has invaded the nasopharynx. Streptococcal skin infections do not cause rheumatic fever. As only approximately 1% of patients with streptococcal pharyngitis develop this disease this indicates that host and environmental factors are of importance.

The average age of onset is 8 years, with an initial attack seldom occuring over the age of 15 years. Patients who have had one attack of rheumatic fever are likely to: have recurrences and these can oc·cur into third decade of life. There is some evidence for a genetic predisposition, rheumatic fever being more common in the offspring of parents ·with rheumatic heart disease than in children of non-affected parents. Poverty and poor nutrition per se do not result in a higher suceptibility, but it is more common in poor communities as a result of environmental factors.

Overcrowding is the most important of these environmental factors. The mechanism by which overcrowding leads to rheumatic fever is probably due to a higher incidence of streptococcal infections as a result of droplet spread between people living in close proximity. Schools in 2 62 the poorer areas also tend to be overcrowded and this further facilitates the spread of the organism in the community. Inadequate primary care

facilities are a contribu~ory environmental factor, as the early diagnosis and treatment of throat infections' prevents rheumatic fever.

INCIDENCE AND PREVALENCE

The true incidence of acute rheumatic fever is unknown as it is often mild or even subclinical. Approximately 30% of patients with rheumatic fever develope rheumatic heart disease. This can be diagnosed clinically • and thus the prevalance of rheumatic heart disease can be ~easured in any community. In South Africa, the prevalence has been shown to be in the region of 7 per 1,000 in underprivileged school children. However, this figure rises to nearly 20 per 1,000 in late adolesence, and this probably represents the adult prevalence of the disease.

CLINICAL FEATURES

The diagnosis of rheumatic fever may be diffucult as it relies not only on clinical, but laboratory criteria.

The Jones criteria are used as a guide in diagnosis. The major criteria are as follows:-

1) Carditis may be diagnosed by the presence of a' raised sleeping pulse rate, cardiac failure or a cardiac murmur not previously present.

2) Arthritis is indicated by the presence of a swollen, painful joint.

Most large joints may be involved, usually in a sequential fashio~.

3) Subsutaneaus nodules have little diagnostic value· as they are usually present in children with severe clinical carditis.

4) Erythema marginatum is uncommon, particularly in dark-skinned races.

5) Chorea occurs predominantly in adolescent females and is characterised by clumsiness, behaviour problems and emotional lability. In more advanced r

63 I 3 \

stages" the patient developes jerky semi-purposeful movements which disappear during sleep.

Minor criteria, i.e. those which are less specific for rheumatic fever, include fever, arthrialgia (pain in joints withiout evidence of inflammat­ ion), a raised erythrocyte sedimentation rate, and a prolonged PR interval on E.C.G. Evidence of previous rheumatic fever is also included as a minor criterion.

In addition, evidence of a recent streptococcal infection should always be sought. This includes a recent attack of'scarlet fever, an elevated antistriptococcal antibody titre or the isolation of a Group A B haemolytic streptococcus from the throat.

MANAGEMENT

Pencillin should be used to erradicate any residual streptococcul infection.

Salicylates (e.g. aspurin) are of great value in the treatment of the arthritis which usually responds rapidly.

Cardiac failure should be treated in the conventional manner with digatalis and diuretics. The use of anti-inflammatory drugs and cortocosteriods in the treatment of the carditis is debatable.

PREVENTATION

Primary prevention involves the treatment of streptococcal pharyngitis, thus preventing rheumatic fever. This in not always possible as patients may be relatively asymptomatic or may not seek medical attention. Easy access to primary care facilities primary prevention.

Secondary prevention focuses of prevention of recurrences in patients who have had rheumatic fever. This takes the form of four-weekly intra- --~~---~

4 64 muscular injections of long-act~ng benzathine penicillin. Treatment should be continued into the third decade of life.

PROGNOSIS

A single attack of rheumatic fever seldom causes sufficient cardiac damage to significantly affect life expectancy. However, repeated attacks of carditis are known to irreversably damage the heart. Prevention of recurrences is thus of the utmost importance. r 65

REFERENCES

American Heart Association. Jones Criteria (revised) for guidance in the diagnosis of rheumatic fever. Circulation 1965; 32: 664-8

Di Sciascio,G., Tananta, A. Rheumatic fever in children Am Heart J 1980; 99: 635-58

Bundred, P. Rheumatic fever. Medicine 1982; 1: 817-20

Bundred, P.,Kitchiner, D. Rheumatic heart disease in South Africa - prevalence and importance. Journal of Continuing Medical Education 1983; 1: 39-45

Portal, R. Mitral setnosis - the picture changes. J'.r Med J 1984; 288: 167-8 66 1

by H M Coovadia, Department of Paediatrics, -", ..~ University of Natal,Durban

-t

I:) - ':"6., .

:1.I, 67

INTRODUCTION

This is a very common disease of children, so much so that by the time an unimmunised child is 4 to 5 years old, he or she would almost certainly have had suffered from measles. It is important for another reason too; it is one of the main killers of children in poor communities.

In South Africa more than 15000 children every year get measles and see a doctor. However the actual number who get measles and do not consult a doctor or nurse is far greater. A similar pattern and number of cases occur each year but occasionally very large numbers of children get the disease and many may die. This is called an epidemic. Between November 19B2 and May 19B3 such an epidemic of measles occurred in the Eastern Cape near Port Elizabeth. Of every 100 children .who got the disease during this epidemic, more than 10 died, this death rate being about 5 or 6 times worse than the situation in a non-epidemic period.

Measles usually occurs in winter,ie between May and September in this country. All children will get the infection if not immunised against it. In the United States of America, there us·ed to be more than 500,000 cases every year before the measles vaccine became available in the 1960's. After the vaccine became routine the number of persons who got the disease fell to a little more than 3000 in 19B1 ie a 99,4~~ reduction. So the vaccine, if properly used can virtually wipe out the disease.

In South Africa there are in gddition racial. differences. Most white children are effectively vaccinated and protected - even if they get the disease it is not severe. Black and Coloured children on the other hand are often not vaccinated and when they get the infection th~ frequently encounter severe problems. For example of every 1000 children who are white who get measles 2 will die, whereas for Indians the number is 5,for Africans IB, and for Coloureds it is 2B.

i ·1, 68

WHAT CAUSES AND SPREADS THE DISEA~ ?

This disease is caused by a tiny germ called a virus which is a primitive organism that can not live on its own but survives by living inside human cells. For those people who are interested, the shape of the virus as seen under a powerful microscope, and some of the parts that go towards making it up, are shown in the accompanying figure.

A person who gets i~fected by the virus gets the disease and passes it on to other individuals. Measles is accompanied by coughing and sneezing, and when this happens, the virus is expelled into the air and is inhaled by another person who is nearby. The virus infects this person in turn and causes measles once again. This process multiplied many times over many thousands of persons causes the spread of measles through a whole community.

If a vaccine has been given it confers protection and the vaccinated child does not get the disease even if exposed to it.

When there are many people staying in the same room or house the vaccine spreads rapidly and therefore all the children get measles at a very young age. Overcrowding also increases the amount of virus that is passed from one person to another. Both these factors ie the young age and the amount of virus passed can cause severe disease. These are Z possible reasons why African and Coloured children get severe measles and not white and Indian children.

PATHOLOGY

Once the virus gets to a child who has not been vaccinated it rapidly gets into many cells in the body and grows there. It also infects the blood. However the main systems which get involved are the nose, throat, air passages and lungs. The bowels, heart, brain and skin may also be infected. Most often the virus causes mild inflammation of the eyes, nose, throat, air passages and lungs. This gets better after about a week and the patient recovers.

When the amount of virus inhaled is very large, if the baby is very young 69

or if the child is malnourished, then the disease causes progressive damage to the lungs and other parts of the body. The lungs can sometimes be permanently damaged so that the child dies slowly over months or years. The bowel can also be affected and if this is severe it causes a"running tummy which if prolonged can also result in weight loss and occasionally death. The brain is rarely infected but may be damaged permanently. The child with brain damage may appear to get better from the measles attack only to die from irreversible harm months to years later.

All this terrible destruction can be prevented by one single injection of the vaccine.

CLINICAL FEATURES

\ Most lay people can accurately diagnose measles. It is recognised by the fl following features: 1) First the child gets fever, cough, red eyes and a runny nose and develops small red spots in the mouth called Koplik's spots. This lasts for 4 days; 2) Next the baby develops a reddish rash which is usually seen first behind the ears and then spreads over the face, neck,chest and occasionally the hands and legs. The wider spread the rash the worse the disease. The rash lasts about 5 days and then fades. When this happens it leaves a brown stain of the skin in some children; 3) In the small number who have this brown staining there is an increase in medical problems. Some of the difficulties children run into with measles are: 1) diarrhoea 2) sore ears 3) sore mouth 4) lung infections 5) infection of th air passages 6) brain problems or encephalitis 7) eye problems - the eye can be permanently damaged.

- + 70

MANAGEMENT

1) Prevention is obviously better than trying to cure the disease once it has struck. All children should be vaccinated. As African and Coloured children get the disease at a younger age than Whites or Indians, the former should get the vaccine at 9 months and the latter at about 15 months.

2) Overcrowding, poverty and malnutrition all make the disease worse. Accordingly these social issues must -be tackled as priorities and especially housing and nutrition improved.

(I 3) Patients need a cough mixture and something to bring the temperature down. Nothing else is required in most children as the disease will get better on-its own.

4) for the very ill, hospital treatment with antibiotics and oxygen may be lifesaving. Dehydration from diarrhoea is treated with oral fluids or intravenous drips.

5) If the lungs are severely affected the sick baby may have to be put on a respirator which is a machine which does the bre~thing for the patient.

CAN ONE RECOGNISE MEASLES WHICH MIGHT BECOME SEVERE?

The answer is yes. The following are hints: 1) Social conditions eg poverty overcrowding and large families -. 2) age - those under 1 year of age 3) malnutrition 4)presence of other serious diseases eg blood cancers 5) rapid breathing,"whooping" or "crowing" with each breath 6) many loose stools 7) fits or extreme drowsiness B) a very sore mouth. 71

BIBLIOGRAPHY

1) Coovadia H. Measles. Kedicine Int 1984;2:20-24.

2) Aaby p,Bukh J, Lisse I and Smits A. Measles mortality, state of nutrition and family structure: a community study from Guinea-Bissau. J Inf Dis 1983; 147:693-701.

3) Coovadia H. Recent advances in the understanding of measles. 5 Afr Med J 1980; 6 : 143-8.

4) Krugman 5, Ward R, Katz SL. Infectious Diseases of children. 6th ed. St Louis: C V Mosby, 1977. pp 132-148.

5; Morley D. Paediatric priorities in the developing world. Chap 12.

~Jndon, Boston : Butterworth, 1978.

.j 0< ~7 ~L .,; o~ Q... -,:j

'"C III 'S' rn 0 ~ 0- , r+- ~ d oJ § U fP ..jl o~ rfl \Il Cl.- 5 a.-~ 3 n E II +' 0 '-..../ d: 0.. 73

.?KIN INFECTIONS

by Z •.Hamed Univ.ersHy. of Natal, Durban

1\ 74

SKIN INFECTIONS

1) SCABIES This is commonly seen and is also known as the "itch". It is caused by a mite Sarcoptes Scabei and produces itchy lumps - especially between the fingers, wrists, elbows, under the-arms, nipples, around the navel, genitalia, buttocks and feet. Infected pustules are seen when scabies has been present for a long time. Eczema and impetigo may also be present. The itch is usually more severe at night and other members of the family may be affected as well. p Scabies is usually contracted from close personal contact eg sleeping together, from using infected towels and bed linen.

The diagnosis is based on a history of severe itching at night - the the rash does not involve the face or scalp in adults. When more than one member of the family complains of itching, a suspicion of scabies should also be aroused.

TREATMENT

Adults'Benzoyl benzoate ( Ascabiol) 200ml per adult. Day 1 - apply to body from neck to toes. After a bath reapply after 10 minutes Day 2 - no bath but apply the lotion to the body. Wait for 10 minutes and apply a second coat Day 3 - bath and no further treatment. Itthiness may last for 14 days Treat all members of the family and avoid overtreatment. Children Under 1 year use Eurax cream - apply to the face as well as the trunk and continue for 4 days Irritation may continue for up to 14 days and repeated treatment should only be advised if there is definite evidence of re-infection. 75

2) BACTERIAL INFECTION OF THE SKIN

I This is known as ~llg£.The commonly responsible bacte~ia are the I' staphylococcus and streptococcus. The lesions have a crust which has the appearance of being stuck on to the skin. Thin walled blisters which rapidly become pustular and rupture are present. The crusts can usually be easily removed leaving a smooth, red, moist surface.

Impetigo usually occurs on the exposed parts of the body - the face, hands and neck. Tender enlarged lymph nodes (glands) may be present. <{ Sometimes a history of insect bites is obtained but impetigo is often :4 ' secondary to head lice, scabies, herpes simplex and eczema. 1

TREATMENT

1) If possible take a swab for bacterial culture prior tp therapy

2) Antibiotics are mandatory and· must be given by mouth. Start with a broad spectrum agent eg erythromycin and continue for a week after clinical healing to prevent relapse. If a swab has been taken the treatment can be changed later if warranted.

3) To the skin apply neosporin ointment three times a day after cleaning well eg with savlon. The crusts should be removed before applying the ointment • Always apply the ointment to the nasal openings.

4) Treat the underlying cause eg scabies or lice. 76

3) FUNGAL INFECTIONS OF THD.SKIN

These may be superficial or deep. The pattern of infection depends on the part om the body involved.

a) TINEA CAPlfIS or ringworm of the scalp occurs mainly in school children and causes 1 or more circular bald patches, mild scaling and redness. The hairs become loose and break off just above the skin surface leaving stumpps.

p) TINEA CORPORIS or ringworm of the body usually affects the face, trunk and arms and legs. One or more sharply circumscribed, slightly red, dry scaly patches are seen. The border is raised and is more inflamed and scaly than the centre. The inflammation spreads outwards and the centre clears.

c) TINEA CRURIS affects the groin usually in men in the hot summer months. It has a curved well defined border and may extend downwards over the thighs or backwards towards the buttocks and around the anus. The scrotum may be involved, 'too.

d)TINEA PEDIS or "athletes foot" is by far the most common fungal disease. Recurrence is frequent. Maceration, scaling and fissures and occasionally blister formation occurs between the toes and under the feet. Secondary

infection is common lead~ng to swollen, infected glands in the groin.

e)The nail is affected by an insidious infectlilon that starts at the junction of nail and nail-bed. A yellow discolouration of the nail occurs and spreads until the whole nail is involved.

Chronic paronychia is an inflammatory reaction of the skinfold around the finger nail. It may be tender and purulent and occurs when the skin is frequently immersed in water eg in washerwomen and dishwashers.

f) TINEA VERSICOLOR is seen as depigmented or pigmented areas on the face, chest, neck or upper arms. Mild itching may be present. After \ treatment sunbathing is necessary to regain the original colour. 77

TREATMENT OF FUNGAL INFECTIONS

To the skin - apply Canesten cream or Whit fields ointment or Castellani's paint to the moist areas.

Oral treatment may be necessary in severe cases. The drug to use is GRISEOFULVIN 1 gram ie 2 tablets are crushed and taken with milk after the main meal daily until the skin is completely clear. This may require 24 months of constant therapy.

'i t 70

BlBLIOGRAf'HY

1) Canizares O. A Manual of Dermatology for Developing Countries. Oxford: O·xford University Press, 1982.

2) Hurwitz S. Clinical Paediatric Dermatology. Philadelphia : W B Saunders, 1981.

3) Verbov J. Modern Topics in Paediatric Dermatology. ", london : Heinemann, 1979. 79

By M Broughton, University of Natal, Durban 80

INTRODUCTION Tetanus has been known for centuries and is commonly

known as "lockjaw". It is caused by a bacteria called ~lostridium Te.lani which produces a toxin (poison) that affects the nervous system resulting in spasms without loss of consciousness. These spasms prevent proper breathing and feeding and frequently lead to death.

Approximately 500,000 cases occur annually throughout the world mainly in the 3rd world - indeed only 81 cases were recorded in the United States of America in 1979. In South Africa tetanus is notifiable by law and roughly one case is reported each day. This is only a small fraction of the true number as most go unreported. The disease affects almost exclusively

,I, underprivileged rural workers and neonates although the incidence amongst heroin addicts is on the increase. In South Africa it is very rare amongst whites who generally receive preventive immunisation. Neonatal tetanus is almost unheard of except in the black community. At King Edward VIIIth Hospital in Durban there are seldom less than 3 or 4 cases at anyone time:

MECHANISM OF INFECTION

The offending bacteria are found in sand contaminated by animal faeces. Infection occurs by contamination of a wound which may vary from insignificant cuts to severe lacerations or burns. The bacteria survive and grow in the soil and dead tissue within the wound.' In the absence of immunity the toxin which is produced may affect the nervous system.

Newborn babies in the 3rd world are frequent victims. They are almost always delivered at home and have had their umbilical cord cut with unclean household utensils ( old razor blades, scissors or dirty knife) The cord may also have been"treated" along traditional lines with soil or cow dung.

~lINICAl FEATURES

Two to 4 weeks after the initial contamination there may be some spasm around the wound • This is followed 48 hours later by stiffness of the jaw, difficulty in swallowing and progressing to generalised muscle spasms. The face is often contorted intoa sardonic "smile". 81

Swallowing and breathing become impossible at times of spasm. Spasms are brought on by any stimulation eg touch, sound or light. They last a few seconds to several minutes and are followed by periods of relative relax­ ation. The patient is fully conscious throughout and obviously becomes very anxious. Further problems are encountered with the control of blood pressure and heart rate.

Recovery in survivors is slow after several weeks of the most distressing illness known to man.

~~NAGEMENT

Prevention is simple and effective and moreover inexpensive. All children should receive immunisation together with their diphtheria and whooping cough innoculations at approximately 4,5, and 6 months fo11wed by further doses at 18 months and before entering school. Boost~rs shou~d be given e~ery 10 years and at the time of severe injury if more than 5 years has lapsed since the last one. It is important to remember that having the disease does not render the patient immune and all sufferers must still be immunised.

Immunisation of pregnant women in 3rd·world countries has dramatically reduced the incidence of neonatal tetanus in these areas.

Further prevention must take place if a wound is contaminated. All foreign material and dead tissue must be assiduously removed and antibiotics given especially in non-immunised individuals. The latter should also receive human serum rich in antibodies against the toxin. This will afford immediate protection against the ravages of the disease. The old horse serum is not used nowadays because of the side effects.

Patients with established tetanus must be refe.red to specialised hospitals where respirators and monitoring equ~pment if necessary in an intensive care unit will be available. Thus a cheaply easily preventable disease is converted anto an expensive catastrophe, often with a tragic outcome.

PROGNOSIS Worldwide the mortality rate of neonates and drug addicts is between 70 and 90%. In the USA this is still 65%. Where considerable specialised expertise of the disease is available eg in Durban the figures 82

are better and have been brought down to between 10 and 20%. However if it is borne in mind that this reflects a vast experience with a potentially preventable disease then the figures are less acceptable and little to boast about.

BIBLIOGRAPHY

1) Blake P A. Serological therapy of tetanus. Journal of the American Medical Association 1976 235 42.

2) Edmondsen RS'and flowers MW. Intensive care of tetanus. British Medical Journal 1979 i :1407.

3) Newe~a K et al. Use of toxoid.io prevention of tetanus neonatorum.

BU~~/etin WHO 1966; 35 : 863.

4) ,Current Pediatric Diagnosis and Treatment. lange Publications, 1982 •. 83

PARA:iITIC: INFESTATION

by M Mackenjee University of Natal, Durban .------~-~~~-~~---

84

PARASITIC INFESTATION

INTRODUCTION

Parasites are organisms which have lost their power of independent life and survive by deriving nourishment and shelter from another organism on or within which they live. Several other organisms or hosts may be used by a parasite during its lifetime, the host being called definitive if it harbours the adult and intermediate if the parasite is immature.

Transmission of parasites from· one host to another~occurs by skin or mucous membrane contact, contamination of food or drink or sometimes through the agency of a vector eg an insect.

The host generally gains little or nothing in exchange for harbouring the parasite ; indeed in most instances the host suffers as a result of the relationship. The effects will depend on the specific type of parasite involved and the anatomical site within the host chosen for settlement.

The prevalence of parasitic infestation is difficult to ascertain accurately. Certainly "worms" in the intestine are so common in children as to almost be considered "normal"; so much so that in some clinics dealing mainly with children from poor socio-economic backgrounds and particularly suboptimal standards of hygiene all children who come to the clinic are routinely treated for certain types of worms. The morbidity of such worm infestation is enormous in the developing world. For example an inverse relationship has been demonstrated between hookworm load and mean haemoglobin levels in rural communities in Venezuela, the anaemia being caused by the loss of small amounts of blood from the gastro­ intestinal tract where the worm attaches. It is estimated that more than 600 million people are affected by infestation with this type of worm alone in the world.

SPECIfIC PARASITES Abrief description will be given of some of the common parasites found in poor people, the clinical features and management of the affected individual.

ASCARIASIS or ROUNDWORM This large pink worm is extremely common and troublesome. The larvae or immature stage are found in the soil where eggs have been deposited 85

usually by contamination with faeces. As soon as an infant starts to crawl there is thus a danger of infection occuring. The larva hatches in the intestine and thereafter migrates through the lung-and back to the intestine where the adult matures.

Vast numbers of these worms can be found in the gut where they can cause intestinal obstruction and colic. When the child is unwell the parasites tend to leave either through the mouth, nose or rectum.

Treatment consists of either Piperazine elixir 3-4grams as a single , dose, repeated after 2 days, or Vermox tablets one, twice daily for 3 days. -\

ENTEROBIASIS or PINWORM This is a tiny thread-like worm that lives in th e large bowel. It chiefly causes irritation in the perianal region as the worm lays its eggs there particularly at night. In females it may enter the vagina and cause a discharge. The diagnosis is easily made by the mother if the perianal region of the child is examined when it is sleeping.

Treatment is with Vermox tablets , one twice daily for 3 days. Preferably the whole family should be treated as cross-infection readily occurs;

Similar features are seen with the worm Trichiuris Trichiura or threadworm. With heavy infestation bloody diarrhoea may occur and anaemia result. The treatment is the same as that for pinworm.

TAENIASIS or TAPEWORM This is less common in children. The infection is acquired from eating contaminated beef or pork particularly if inadequately cooked. The diagnosis is made when the flattened segments of the worm (O,5X2,Ocm in size) are passed per rectum.

Treatment is with Yomesan, 1 tablet for every year of age up to a maximum of 4 tablets. No eating is permitted for 2 hours thereafter. Vermox one tablet twice daily -for 3 days may also be effective.

SANDWORM This is a dog carried hookworm that penetrates the skin in the larval form . After maturing it migrates along the superficial layers of the skin causing a "creeping" eruption. An ointment comprisin§ Thiabendazole applied to the skin is effective. 86

BILHARZIA This is picked up when a human enters water contaminated by a specific form of snail which harbours the bilharzia parasite or Schistosoma. The immature stage or cercaria penetrates the skin and matures as an adult in the liver. From there it either migrates to the large intestine or urinary tract ( depending on the type ) where it lays eggs and the cycle continues. In the intestinal variety, diarrhoea with blood is the common problem while if the urinary tract is mainly involved the main sign is blood in the urine. Diagnosis is based in the finding of eggs, either in the stool, urine or through more invasive procedure eg a rectal biopsy. Long term complications c~n occur eg urinary tract obstruction and kidney failure.

Treatment of the affected person is now easily ana safely achieved with the use of Praziquantel 25mg/kilogram body weight. -Prevention of the disease is perhaps the better way of tackling the problem with the erradication of the parasite-harbouring water snail being one way of breaking the cycle.

AMOEBIASIS The parasite can live either in the intestines or extra-intestinal site of humans. Of the latter the liver is perhaps the most important. If the intestine is mainly involved then the patient presents with bloody diarrhoea ( dysentery). If the liver is involved then a major problem is that of abcess formation which may grow to an enormous size and cause significant morbidity. In both instances the tratment which is extremely effective is Metronidazole ( Flagyl) tablets for 5 days. There are few side effects of this extremely useful drug.

~ It is difficult to discuss all the parasites that affect man as each is different and demands a different approach. A useful reference for many common South African parasites is: CLINICAL MEDICINE AND HEALTH IN DEVELOPING AFRICA edited by G D Campbell, Y K Seedat and G Daynes, published in Cape Town by David Philip, 1982. 87

DISABILITY AND HANDICAP

by Pet.er Disler Department of Community Health, VCT 88

Disability is defined by the World Health Organisation (WHO)I. as " ••... any restriction or lack (resulting from an impairment) OL the ability to perform an activity within the range considered normal for a human being." Handicap, in the same publication is seen as " .•• a disadvantage resulting from a disability that limits or prevents the fulfilment ofa role that is normal (depending on age, sex and social and cultural factors) f~'l"' that individual." The distinction between these two states is critical. It is often the environment, notably social and economic elements of it, that transform disability into handicap. An example of this to which many of us can personally relate is shortsightedness. This condition, so common as to almost be considered "normal" in our society is usually based on a fixed irreversible disability which can be totally corrected with the prescription of the correct spectacles. If these are not available, perhaps through lack of local technical expertise or inadequate funds, the disability becomes a handicap, perhaps so severe as to prevent work or even mobility.

The prevalence of disability. The wide terms of reference of disability make accurate assessments of prevalance difficult. Based on a comprehensive literature review, the WHO has stated that "no more accurate an estimate can be amde than that the disabled comprise about 10% of the world's population."I. The major manifestations are blindness, deafness, mental illness and retardation, general physical debility (usually locomotor impairment) and addiction to alcohol and drugs. The major causes of disability and the estimates of global ~revalence are given in Table 1. 89

TABLE 1

, Estimated No in the % of total auses of Disability World (millions) disability

ongenital 100 19,3 ommunicable diseases 56 11,0 Non Communicable somatic 100 19,3 diseases < , IFunctional psychiatric 40 7,7 Alcohol and drug abuse 40 7,7 ~~ 78 15,2 ~"'"""i'i"" 100 19,3 Other 2 0,5 516 100

The final figure of 400-500 million or 10% of the 4 000 million people in the world at the time of the estimate, is conservative and excludes about 25% who might fall into more than one category. It is further estimated that at least 50 million of these disabled people live in 2 Africa and 80% in developing countries. .

An important projection from these data is that the disabled population is increasing by at least 3 million annually and that by the year 2000 the figure will exceed 600 million. Although up to half of these people would be expected to benefit from rehabilitation, only 1-2% have access to such facilities.

If the definition of disability is narrowed to those who for this reason cannot participate in an activity such as school, housekeeping or work,the estimates are lower, in the region of 3-4%. Depending on the definition used therefore there are probably between 1 and 3 million disabled South Africans. Another important element is however the elderly, many of whom are severly disabled but often excluded from the estimates. Ours is an ageing population, the number of elderly ... ------~-~-~-~- --

90

in the white community reaching approximately 8% at present. With develop- ment this figure is expected to increase and may cause further escalat­ ion of the problem.

Poverty an~'disability. It is well known that disability is more common among the poor. In the USA, the Census Bureau found that in the economically active age group, 28,7% of poor people were disabled in comparison with 11,8% of the less impoverished. Predictably, race entered the discussion, 17,6% of American Blacks being disabled and only 13,7% of whites.3 .

Whether poverty leads to disability through greater susceptibility to causes in the domestic, social or working environment or disability aggravates poverty by limiting education and earning power is subject

to debate. The latter is fav~ured by many authors. Irrespective of the sequence, poverty and disability together produce a disastrous effect.

Management. As the clinical features will depend on the type of disability and be obvious in most instances this will not be dealt with further. The'principles of management will be outlined emphasis­ ing limitation of cost a~d appropriatness to Doverty and curtailed resources.

Primary prevention. Prevention,of disability is dependrnt on erradicat­ ion of the causes mentioned earlier. It is hoped that strategies for some of these, particularly poorly related, will emerge at this coriference~ It should be noted, however, that the situation is urgent,as with respect to the three major causes of disability in developing countries viz.

malnutrition, communicable diseases and accidents, all are ~ctually on the increase and inadequately addressed.

Education must be at the root of any programme however, both general and health related. In this respect much greater advantage must be 91

taken of the resource of lay people; skilled expertise is hard to come by and expensive.

Secondary prevention. this inc~udes early diagnosis and "cure" of established disability. An important field in this respect is blindness which can so often by managed surgically. It is important to. stress that we must move away from central "centres of excellence" which consume so much of the budget particularly in the 3rd world. Mobile and static rural clinics and small hospitals can do much to ease the load of established disease. Screening programmes are also essential if the consequences of established disability are to be avoided before it is too late.

Tertiarv prevention. Even if primary and secondary prevention receive adequate attention in the near future, which is perhaps a naive hope, the number of people with already advanced disability is enormous. This element of care i.e. rehabilitation thus remains a priority.

If a rational service is to be established then the needs must be determined. It must be stressed therefore,that these are not only as perceived by medical personnel but by the disabled themselves. The past ·few decades has seen the development of a vocal and articulate body of disabled people, unhappily but logically poised to identify problems far better than we can. This has partically flourished in America, sadly an offshoot of the Vietnamese conflict, but has now spread to Sou.th Africa where" Independent Living Centres have now been started in both Johannesburg and Cape Town.

; The key to rehabilitation is perhaps access; access to education, access to occupation and through it vital reso~rces and access to recreation. This requires the development of aids and these can often be manufactured 92 locally, using local expertise and at low cost. At the forefront of research is AHRTAG, Approach Resources and Technologies Action Group, based in London and directing development projects throughout the world. Wooden chairs can be converted into wheelchairs, crutches made of local wood and even spectacles made on machines driven by "pedal power". Moreover, local, relatively. untrained personnel can be used to manu­ facture most of these. Integral to this is an attitudinal change among ablebodied people, to allow disabled individuals to penetrate and take part equally in our ftchievement orientated society.

Access to work is a vital element, allowing a disabled person to survive independently. In South Africa, legislation exists for the subsidisation of the salary of a disabled person by the state for up to 3 years (80% in the first and ~ecreasing to 40% in the third). Nevertheless employers are loathe to take the chance on a disabled individual. They too need education. If work is not possible, state pensions are available but then are pitifully low and moreover racially discriminated varying from RS7 per month maximum in Blacks, through R93 per month for Asiatics and Coloureds and RlS2 per month for Whites. A further RIS per month attendence allowance does little to make these amounts meaningful.

It should be stressed that a network of welfare organisations and admirably motivated people are active in the community in the field of disability. What is lacking is a concerted endeavour, bringing together the skills and will of all those .involved and leading to a rational programme which will allow disabled people to achieve their right of equal participation within society. 93

REFERENCES

1. WHO Tech Rep Series, No. 668. Disability prevention and rehabilitation. Geneva: WHO, 1981.

2. Collet, A. International cooperation. In: Education and Rehabilitat- ion of the disabled in Africa, ed. K. Marfo, pp. 207-216. -i Canada : Centre for International Education and Development, 1983.

3. De Jong, G. and Lifchez, R. Physical disability and Public Policy. Scientific American 248.: 26-36, 1983.

4. l)ick, B., ·Wolfe, E., Watermeyer, G.S., et a1. Chronic illness in non­ institutionalised persons. South African Medical Journal, 53 892-904, 1978. 94

OCCUPATIONAL LUNG DISEASE

by Derek Yach 1. an d J onny Myers 2.

1. Department of Medi"cine, liCT. 2. Industrial Health Research Group, Department of Sociology, liCT. 95

INTRODUCTION

Occuaptional lung diseases (OLD) are regarded as the group of pathological lung changes caused by the inhalation of injurious substances during the course of employment. 1. Major group·s of aI.bstances include mineral dusts, organic dusts, gases and fumes. From Table 1, which contains the number of workers exposed to major toxic agents in South Africa, it is apparent that hundreds of thousands of workers are exposed to-agents in the workplace capable of producing lung diseases. This chapter will briefly outline the types of diseases produced by these agents, the methods and problems of diagnosing these diseases and compensation abailable to workers adversely effected. Asbestos-related diseases and lung diseases caused by grain dust exposure will be used to illustrate certain problems associated with managing OLD's in South Africa.

Diagnosis

The types of diseases produced by commonly encountered agents are shown in Table 2. For many of the listed diseases, diagnosis requires no more than an adequate occupational history, basic clinical examination, l chest X-Ray and pulmonary function evaluation. . Despite this, the specific occupational origin of many workers'dise8se often goes unnoticed especially if there is a '~ack of official awareness of, or concern for the health of workers.,,4. Frequently, factory doctors' identification with their employer first (i.e. not workers) leads to underdiagnosis of OLD. Workers in South Africa are exposed to several hazardous substances that have been restricted, controlled or banned in developed countries. Reasons for their use in industry in South Africa are, firstly the relatively cheap cost of local labour, secondly the lack of industrial legislation and thirdly, the absence in many cases Qf strong union pressure. Lately, unions have started to support industrial health research into the effects of substances like asbestos, cotton and grain dust. .------

96

Another reasons for the underreporting of OLD is that many workers are lost to follow-up once they leave their workplace. Many migrants only become ill once they have returned to their'rural home. The connection between the disease, su"lsequently,diagnosed in such rural areas, andits industrial origin is often missed'. This has obvious implications for compensation.

Pneumoconioses

Pneumoconioses are the most frequently contracted occupational disease in South Africa. Workers 'in primary, industries like mines, quarries and foundries as well as secondary manufactury or processing industries are at risk of developing miners dust related diseases. In the Erasmus Comm:i..ssion it was 'estimated, that 25% of workers exposed to mineral" dusts develop pneumoconioses. Despite a decline'in the silicosis death-rate,

,the incidence (of new cases) has incr~ased.

Most pneumoconioses are diagnosed' by comparing full size chest X-Rays to standard International Labour Organisation X-Rays.s. The few factories where X-Rays are done, mini XRays are usually taken. These frequently do not detect pneumoconioses. Diseases like asbestesis and silicosis lead to restrictive lung diseases i.e. the lungs become scarred and shrink. This results in increasing breathlessness on exertion.

Obstructive Disease

In contrast to mineral dusts, organic dusts like those of cotton or grain produce an obstructive pattern. The lung size is usually not reduced but the time taken for normal expiration is increased. Symptoms typically include whezing, tightness and breathlessness. In the case of byssinosis, 6 symptems are usually worse after the first shift of the week. . Agents like wood dust and grain dust can cause bronchial asthma - a ,reversible obstructive lung disease. · '

97

Tuberculosis

Tuberculosis appears on Table 2 as an OLD. Considerable evidence suggests that several occupations, especially mining, lead to a reactivation of

latent TB. Not only dust exposure in these occuaptions leads to a~ increased TB risk. The general fatigue and stress among nutritionally comprised miners significantly inceases their TB risk. Migrants diagnosed as having TB, are sent back to the "homelands" wi thout treatment. This could partly account for the very high TB incidence rate in SA (i.e. 60 000 new cases annually notified).7. Tuberculosis can coexist with silicosis and result in a particularly lethal outcome. For example, it was shown in 1960 tha't most patients with silico-tuberculosos died within two years of diagnosis. This combination of diseases is recognis'e<;l by the Workers Compensation Act.

Asbestos-related diseases

In South Africa, 22 000 miners in 1977 were known to be exposed to asbestos dust. Several thousands'more handle, rrocess or use raw asbestos or asbestos products, i.e. insulators, builders, boilermakers and shipyard' workers.8 . All these"worker's are at, risk of dev'eloping' asbestos, lung cancer, mesothelionia and GIT cancers. Since 1932, measures were taken to reduce asbestos fibre exposure in Britain but it took a further twenty years before health surveys in South Africa showed the effects of ,asbestos mining on health. Even children less than twelve years ago who worked as asbestos miners showed evidence of asbestosis. Later work by Wagner resulted in the first published accounts linking environmental asbestos --- -. ---, - -, - 9 ------exposure to the 'development of, mesothelioma •. Despite these and sub- sequent research results, there are still no statutory levels for asbestos fibre in South Africa.' Instead, the Department of Mines suggested that levels of 5 fibres Iml be applied from 1982. (Current British standard for Blue Asbestos is_ 0,12 fibres/ml). No minimum threshold level for asbestos below which cancers do not occur have been found. 98

Asbestos-related conditions (excluding lung cancer) account for 53% of all white miners pneumoconiosis compensations and 52% of all notified mesothelioma cases are whites (whites represent 5,4% of the asbestos labour force). In sharp contrast, Africans who form 91,6% of the labour force 8 accounted for only 28% of mesotheliona notifications. . The undernotification of Africans represent the lack of case finding and the fact that since mesothelioma has a "iatency of 5 to 40 years, many migrant workers are 'lost' in the Bantustans to follow-up or are mismanaged.

Grain dust diseases

A total of.56 000 workers in South Africa are exposed to grain dust. These include workers in grain mills, transport services and bakeries. Grain dust causes a range of diseases including bronchial asthma, chronic bronchitis and grain fever. lO • It is estimated that 2-15% of all asthmas ll are occupationally related and up to 20-30% of bakers develop asthuma. . Asttmo develops after a period of symptomless exposure that may vary from weeks to years. Unlike in Britain where grain dust and flour are recognised tor compensation purposes as one of seven groups of industrial agents 12'capable of producing asthma, occupational asthma is not compensat­ able in South Africa.

Chronic bronchitis is common among these workers and occurs independently of their smoking habits. Despite this, workers 'smoking habits are often used as a scapegoat and given as the reason for their disease. Similar arguments have been used in the case of cotton workers. As with asbestos, no stat~.tory_ grain dust levels exist in South Africa.

Compensation and legislation

Current legislation contains no statutory. limits for agep.ts such as dust, fumes or gases that cause OLD. The legislation, tlteMachinery and ------~~------

99

Occupational Safety Act of 1983, is vaguply ~orded and leaves enforcement to the discretion of the factory inspector. In 1975 it was estimated that only 29 of 66 factory inspector posts were occupied and that 30 000 factories in South Africa required inspection 2. i.e. enforcement is totally inadequate. The 1983 legislation has entirely disregarded the major recommendations of the Erasmus Commission2. made nine years ago calling for all occupational health and safety legislation to be placed into one Act and be administered by one State department. Occupational health now falls under the departments of health and manpower. Furthermore, the legislation has made no provision for worker/union participation in determining and monitoring health standards in industry.

Table 2 shows that only a limited number of recognised OLD's are included in the schedule of diseases approved for compensation in South Africa. Striking ommissions are lung cancer (especially for asbestos, uranium and chrome miners) and occupational asthma. Workers can apply for compensation for non-scheduled diseases if they can show that their exposure led to the disease , i.e. the onus is on the worker to prove that agent X causes disease Y. In_ reality this rarely happens, since most workers are not informed about the effects (especially longterm ones) of agents in their workplaces. Bureaucratic procedures are a major cause of delay in obtaining compensation for scheduled diseases. The maximum payable (to those who are 100% disabled) under Workman's Compensation is three-quarters of a workers' monthly earnings up to R400/month-and half of the ammount over R400. This is not payable for the first three days and, unless special permission is obtained, is us_ually payable only for one year.

Finally, it is imperative that a stategy that includes the setting of health standards; engineering controls to reduce exposure to toxic agents; worker education; preventive diagnosis; professional training and workers' compensation be urgently implemented so that the high prevalence of OLD can be reduced.

. ;- 100

TABLE 1 THE NUMBER OF WORKERS EXPOSED TO AGENTS THAT· CAUSE OCCUPATIONAL LUNG DISEASES IN RSA, 1979

Number of Workers Exposed

(miners) 21 665 \. 589 672 175605 165 777 10 486 (baking and milling) 43 000 89 826 52 185 ilica (all mining) 445 240 extile spinning and weaving 86 400 awmills and furniture factories 37 271

Source Erasmus Commission, 19752: TABLE 2 COMMON OCCUPATINOAL LUNG DISEASES IN SOUTH AFRICA

i f Category Special Agent ! Diseases JlCompensation in South Africa

Mineral Dusts Coal Coal-workers' pneumoconiosis Yes Asbestos Asbestos, lung cancer, pleural mesothelioma Yes, but not lung cance Iron Siderosis Yes Chrome Lung cancer No Silica Silicosis Yes

Organic Dusts Cotton Bysinllosis Yes Grain Grain fever, asthma, chronic bronchitis No Wood - Asthma, chronic bronchitis No . Gases and Fumes Ammonia Acute bronchitis, chemcial pneumonia No Ozone Chronic bronchitis No

Other Mouldy Hay Farmer's fung No , \ Sugar cane I Bagassosis No TB bacillus Pulmonary tuberculosis No

Source: Levy, 19833.; Erasmus Commission, 1975.2•

...... <:>......

___..... ~ m _=il'ihialz bU4 £ZlED2 .--...... ------~<------~---

102

REFERENCES

1. Campbell, G.D., Seedat, Y.K. and Daynes, C. Clinical Medicine and Health in Developing _

Africa, < David Philip, Cape T~wn, 1982.

2. Report of the Erasmus Commission of Enquiry into Occupational Health, Government Printer, Cape Town, 1975. (R 295).

3. Levy, B.S., and Wegman, D.H. Occupational Health, Little, Brown and Company, Boston/Toronto, 1983.

4. Pennel, I., and Doyal, L. The Political Economy of Health, Pluto Press, London, 1979.

5. Brooks, S.M., "The evaluation of occupational airways disease in the laboratory and workplace",-_~ Clin Immunol, 70: 56-66, 1982.

6. Wegman, D.H., Levenstein, C., and Greaves, I.A. "Byzssnosis : A role for Public Health in the Face of Scientific Uncertainty", AJPH, 73 : 180-192, 1983.

7. Department of Health, "TB- Incidence by Population Group, RSA, 1972-1982", Epi Com, 10 : 3-9, 1983.

8. Myers, J. "The Social Context of Occupational Disease: Asbestos and South Africa", Int of Health Scrv, 11 : 227-245, 1981.

9. Benatar, S.R., and Bateman, E.D. "Editorial: The asbestos hazard", S Afr Med J, 62 : 881-882, 1982. 103

10. Cotton, D.J. and Dosman, J.A. "Grain Dust and Health. 1. Host factors", Ann Intern Med, 88: 840-841, 1978.

11. Editorial, "Baker's Asthma: Development and Possibility for Treatment", Chest, 78- : 400-405, 1980.

12. Hendrik, D. and Fabbri, L. "Editorial: Compensating Occupational Asthma", Thorax, 36: 881-884, 1981. .------~~-~- ~~~------

104

HYPEIITENSION IN soorn AFRICA

by Chippy Olver SALDRU. U.C.T. 105

HYPERTENSION IN SOUTH AFRICA

INTRODUCTION

The human body ·responds to stress through a physiological arousal mechanism that activates the sympathetic nervous system and releases certain hormones into the blood stream. The immediate effects are a rise i~ blood pressure and heart rate, and increased alertness. This is the 'fight or flight' response - a Preparation for whatever action is deemed necessary in a stressful situation. In a modern society, however, this response is not always appropriate frequently we can neither attack nor run away from the stresses of our lives. They are continually with us, within the very nature. of our society. In this situation a continuous activation of the stress response becomes quite harmful.

DEFINITION

Hypertension is·an abnormally elevated blood pressure. The contraction and relaxation of the heart ·give us systolic and diastolic pressure read­ ing~, expressed in terms of millimetres of mercury (mmHg). Both values may be raised in hypertension. The World Health Organisation has defined hypertension . as present if the blood pressure readings are greater than or equal to the following values:

~ Diastolic SIstolic Under 30 years 150 mm Hg 90 mm Hg Over 30 years 160 mm Hg 95 mm Hg

Over 65 y~ars 165 mm Hg 95 mm Hg 106

THE NATURE OF THE PROBLEM

Hypertension is, classically, an 'epidemic' of modern industrialized societies. Within the United States 15% to 20% of adults are affected. l • Why then have we included this disease in this booklet? A closer examination of prevalence studies reveals that it is not the upper middle-class executives who are primarily affected. The main target group are the urban blacks, who have twice the prevalence-rate of hypertension, and four times the hypertension-induced disease rate than their C3ucasian counter- parts.I. This has often been ascribed to genetic factors, quite over­ looking the fact that blacks in the USA are one of -the most oppressed and exploited groups in that country. Data for South Africans is scarce, but a number of isolated studies allow us to build ~p a picture of the situation:

Mean blood pressure values for blacks in Johannesburg and whites in London have been compared - the JHB figures were consistently and markedly higher than the London figures. 2• A survey of black work-seekers in JHB showed an incidence of approximately 30% in people over the age of 30 years - the 50 to 59 year age-group had on incidence of approx­ imately 40%.3.

A study of hypertension in Durban gave the following (age-corrected) figures:

Zulu 25% Indian 14,19% White 17,2%

Both black and coloured dock workers were surveyed in Cape Town. 43,9% of those surveyed were found to be hypertensive. There was no significant difference between the race groups.5 •.

The incidence of hypertension amongst rural blacks is lower than the urban values for any group. It has been estimated at 7% by the minister of health and social welfare for Bophuthatswana.3 • This 107

bears out another study in the Transkei which found an incidence of 8%~· A study in rural KwaZulu found an incidence of 10,5%.6. Obviously· genetic factors cannot account for the extremely high prevalence of hypertension amongst urban blacks in South Africa.

THE CAUSES OF HYPERTENSION

These and other studies have revealed that the following factors are associated with hypertension:

1.~. Blood pressure. levels climb steadily at the work-seeking age, and are particularly high in the 50 year old age group.

2. Sex. Women usually have higher prevalence rates than men.

3. Obesity.

4. Marital Status.Widow/ers and separated persons are more frequently affected.

5. Urbanization. Prevalence increased in relation to the number of years spent in the city.

6. Number of Dependants.

7. A family history of hypertension, diabetes or stroke.

The following factors were found to be important in urban populations. 1. Smoking '.

2. Alcohol

3. Working conditions, especially in terms of overload and underload.

4. Occupational social class. lOB

5. A level of education below Std. 2':

6. Incomes below RlOO/month for men R 40/month for women.

7. Unemployment.

8. Number of unemployed children.

9. A lack of recreational or sporting facilities.

10. Overcrowding.

11. Insomnia due to anxiety.

CLINICAL ASPECTS

In the vast majority of cases hypertension is symptomless. It is usually discovered as an incidental finding on clinical examination. In severe cases it may cause headaches, dizziness, blurring of vision, fatigue and palpitations of the heart.

The implications of this 'sih;nt' disease, however, are quite severe. There is a direct relationship between blood pressure levels, and death rates.l.

Untreated, hypertension is associated with a shortening of life by 10 to'20 years, and an acceleration of atherosclerosis (which is a hardening of thear.terywa11s, itself causing many comp1ications).1. After 7 to 10 years nearly 30% of cases will exhibit complications of atherosclerosis and more than 50% will have end organ damage in the kidneys, heart, retina of the eye, or the brain. l • 109

If the systolic pressure is greater than 180 mm Hg, or th~ diastolic pressure is greater than 110 mID Hg, the associated mortality is markedly increased. In very severe cases the disease becomes progressive, and is knew;l as 'accelerated.' or malignant hypertension.

The major complicattQn of hypertension are:

1. heart failure

2. ischaemic heart disease ~nd heart attack

3. kidney failure

4. stroke s. cerebral haemorrage.

Because these complications are so prevalent in South Africa, hypertension is one of the major killers amongst urban blacks. Within the cities hypertension is not only more prevalent than the rural areas, it is also more severe, and has a higher associated mortality.

TREATMENT

The treatment of hypertension is extremely problematic. The majority of cases remain undiagnosed, and untreated .(The Cape Town dock workers study revealed that 8,1% had been diagnosed, and 4,9% had been treated). Treatment is often life long, and requires considerable motivation of the part of the patie~t. Compliance is thus an enormous'problem. A study at the Soweto polyclinic7 . showed that only 27% of patients put on treatment man~ged to get sufficient (80%)' medication. Transport costs and travelling time to and from the clinic are probiems.

Further it has not been adequately proven that treatment of mild forms of hypertension, even over a ten year period, significantly reduces the associated mortality. For severe cases (diastolic pressure greater 110 or equal to 100 mm Hg) treatment significantly reduces mortality, and consists of the following:

1. General measures.

a. relieve stress (relaxation techniques)

b. dietary control

i) restrict salt intake ii) restrict energy intake iii) avoid cholestrol and saturated fats

c.. exercise

d. stop smoking cigarettes.

2. Drugs

These are added stepwise in the following order until the blood pressure is controlled.

a •. diuretics ~.

b. agents that block the sympathetic or hormonal stress response

c. agents that dilate the artery walls.

d. agents that depress the central nervous system.

'The magnitude of the problem requires a,fundamentally new approach to combating this disease. The.need to involve the community has been repeatedly emphasized. Clinics, situated within the comm~nity, and .primary health care nurses must become the main line of attack. The diagnosis of hypertension is easy, and can be carried out by a lay person with a minimum of training. On a ~ider scale, efforts can be made to alter individuals lifestyles; especially their diet, smoking, alcohol intake and exercise. But this is a'classic victim­ blaming approach, and inevitably masks the real causes of the problem. Further, the problems of an unhealthy lifestyle are themselves symptoms of a greater problem. 111

THE ROOTS OF THE' PROBLEM

90 -' 95% of hypertension cases have !!2. obvious cause (e.g. kidney disease). It appears that hypertension is the result of continuous psychological and physical stress imposed on the individual by the environment in which we live and work, and mediated by specific features within an individuals lifestyle and immediate social network. The s~urce of that stress is very much related to the nature of South African society. The following processes are implicated:

1. The transition of the rural peasantry from a self-sufficient populat­ ion into a migrant workforce.

"Colonisation, conquest and the development of' capitalism in South Africa have led to the complete undermining of the pre-capitalist mode of production. The period since the turn

of the c~ntury has seen the evolvement of the broad mass. of \. agricultural producers into a pri etarian workforce dependent. on wage labour for its subsistence. The pace of social change which has been accelarating continuously has now become tremendous.

Urbanisatiqn,e~iction of labour tena~ts, resettlement and growing dependance on migrant labour have all contributed J. ~ ~ . '1 .f "'!-' ~ t to the break-up of stable family'ties and supportive social structures. H2 •

2. The nature of work for the working class: Within a:capitalist economy the drive1to increase profits takes precedence over the well being of the workers concerned. Profits can be increased ,by:

a) 'increasing the working day - this results in exhaustion and fatigue, and deprives people of the relaxation time necessary to form stable social relations.

b) decreasing wages - poverty is without doubt one of the greatest stresses with which any individual must contend. 112

c) increasing the productivity of labour i.e. by increasing the mechanization and pace of work, and introducing further specialization of tasks such that the worker ends up with a monotonously boring job. The worker has progressively lost control over the work that he does, and is s?bjected to the pace of the machines that he operates. Organisation at the work place, e.g. trade unions is continually undermined by the bosses and the state.

3. Conditions within·. .'the urban townships. Poverty, overcrowding and unemployment are stresses that have created appallingly high crime rates and alcoholism, themselves added stresses. Pass raids and police harassment are everyday occurrences, where apartheid is a harshly oppressive reality. Outlets, such as sporting and recreational facilities, are scarce or absent.

In summary, we do not have to look very far beyond the individual to ascertain the causes of hypertension. 'The fabric of our society is fraught with alienation and fractured social relations. Obviously there can be no simple solutions to the problem. As a beginning, we can attempt altering the patterns of control within our society. The most stressful situations have been shown to be those where the individual concerned has no control over the processes taking place. Within South Africa, the majority of people not only have no political franchize, they also have no say over the work that they must do, no say over the organization and administration of townships and social services, and whatever democratic organisations they attempt .to form are invariably harassed, intimidated or banned by sections of the state apparatus. We must seek a democracy, and not just representative democracy, but a thorough-going participatory democracy, where the word 'community participation' becomes more than just rhetoric on the part of administrators. But we must go further than this. Alongside a democratization of our society must go fundamental changes in the patterns of wealth and ownership, so that the productive forces of society can become a source of wealth for all, and not of arduous toil and· exploitation. 113

and exploitation . We must seek - ..... "the slow transformation of the very nature of labour from a coer~ive necessity in order to get money, income and means of consumption into a voluntary occupation that ,people want to do because it covers their own internal needs and expressed their talents. This transformation of labour into an all-sided creative human activity is the ultimate goal of socialism." 9 'The Causes of Alienation' - E. Mande1. . 114

REFERENCES

1. 'Hypertension Vascular Disease' - G.H. Williams, P.I. Jagger, E. Braunwald, pub!, in Harrison's "Principles of Internal Medicine", 9th ed. 1980.

2. 'Hypertension, Stress and Social Organisation in South Africa' - Neil White, publ. by Health Care Trust

3. Papers delivered at a workshop on hypertension, published in SAMJ 14.6.1978.

4. 'Hypertension and ischoemic heart disease in Indian people'living in South Africa and in India' - Y.K. Seed at , publ. in SAMJ, 19.6.1982.

5. 'Prevalence of hypertension in semi"':skilled manual workers' - J.E. Myers, N. White, J.E. Cornell, -publ, in SAMJ 4.12.1982~

6. 'Biosocial factors and hypertension in urban and rural Zulus' Y.K. Seedat, M.A. Seed at , D.B.T. Hackland, SAMJ 26.6.1982.

7. 'Hypertension management and patient compliance at a Soweto polyclinic' _ L.D. Saunders, L.M. Irwig, T.D. Wilson, SAMJ 30.1.1982.

8. 'Aspects of hypertension among blacks' - K.P. Mokhobo, SAMJ 12.6.1982.

9. 'The Causes'of Alienation' - Ernest Mandel. 115

i I

'. , -

ROAD TRAFFIC ACCIDENTS

by Noddy Jinabhai, Department of Community Health, University of Natal, Durban.

, ' . -

, '. 116 ROAD TRAFFIC ACCIDENTS

Introduction

2 Epidemiology of t~affic accidents 3 Interventive measures 4 Bibliography

INTROIllCT ION

In 1983 there were over 388 000 traffic accidents involving over a

100 000 casualties and 9121 persons being killed (Table 1). Human miserY and suffering. loss of life. loss of bread winners. economic crises in families due to death or,.disablement. loss of human resources and sk ills to the country and the vast sums expended on hospital treatment and subsequent care of the disabled - all these are the consequences.

,.' 117 , TABLE 1 SUMMARY OF ROAD TRAFFIC ACCIDENTS - RSA (19.83)1

t Accidents fatal 7 941 major 18.653 minor 49 017 no injury 312 988 Total 388 599

Casualties Total, 106 457

Killed driver 2 507 passenger 2 S60 pedestrian 4 054 Total 9 121

Seriously injured driver 8 862 passenger 10 002 pedestrian 8 763 Total 27 627

Slightly injured driver 2& 625 passenger 23 S28 pedestrian 17 SS6 Total 69 709

Road vehicles involved - total 657 756 118

The two graphs (Fig 1,2) reflect the rising trend of all r~ad accidents and the persons killed during the yea~s 1979 - 83. 1 It is estimated that 'traffic accidents constitute 5% of all deaths reported in South Africa. 2

The age-specific casualty' rates are highest in Whites in the age group . 1 15 - 34 years (Table 2 and Fig 3) and lowest amongst the Africans. The mortality rate as a result of motor vehicle accidents (MVAs) is highest amongst pedestrians followed by passengers, drivers and pedal .. cyclists (Fig 4). The actual MVA mortality .shows that Africans had the highest mortality (62,5%) followed by Whites (21,O%), Coloureds (13,5%) and Indians (3,0%). (Table 3)2

TABLE 2 MVA MORTALITY BY STATUS AND RACE - NUMBER AND PERCENTAGE

African White Coloured Asian pedestrian 3 139 (34,6) 155 ( 1,8) 693 ( 7,6) 78 (0,9) pedal cyclist 317 ( 3,4) 62 ( 0,7) 59 ( 0,7) 5 {O,n passenger 480 (16,3) 544 ( 6,0) 320 ( 3,5) 104 { l,n driver 741 ( 8,2) 140 (12,5) 158 ( 1,7) 82 (9,9) Total 5 677 (62,5) 1 911 (21 ~O) 230 (13,5) 269 (3,0)

9 087

; l 119

I, 2 EPIDEMlOLOGY OF TRAFFIC ACCIDENTS I

The multiple factors ~ssociated with road traffic accidents can be sought in relation to man, agent and environm'ent. 3

FACTORS RELATED TO MAN alcohol intake fatigue and frustration inadequate/immature personal ities, of drivers diminished mental and physical reflexes of the aged visual, hearing, metabolic defects and diseases side effects of drugs

FACTORS RELATED TO AGENT (VEHICLE) brakes steering tyres 1ights speed

FACTORS RELATED TO ENVIRONMENT - state of loads visibil ity road signs traffic control

It is self evident that these factors operate within a given social milieu - the nature of society, its ethos and value systems, the economic value of the commodities involved (cars, alcohol etc) in comparison to the human costs incurred would be reflected in the toll 120

in casualty rates (morbidity) and mortality from traffic accidents.

This toll is part of a broader spectrum of social diseases related to an acquisitive. individualistic and consumer orientated life style of individuals (and society) - and includes conditions such as depression and suicide. stress related diseases of ischaemic heart disease and hypertension. alcoholism and drug abuse and syphilis and malnutrition.

Despite the good intentions of the State and bodies such as the National Road Safety Council (NRSC) for meaningful progress to be achieved. the collective interests of society (to control and.

eradicate thi3 epidemic) must be given the sa~ priority as individual freedom (to maim and kill). The hidden costs to society for such symbols of affluence and development must be explicitly stated and community opinion mobilised to control them.

3 INTERVENTIVE MEASURES

In a general sense. at the conununity.level. the necessity. for',acari-ng and conununity supportive society is critical for any legislative. judicial. medical and economic sanctions to be effective. In such a society the value accorded to human lives must be greater than the

search for profits and social forces generated within. society mus~ ensure the dominance of the former over the latter.

The interception of factors at the specific level of man, agent and environmental factors are more likely to suceed within the above context. At the subjective. personal level - re-education through all the media 121

in respect of a new value system, the dangers inherent in and the /' correct handling of motor vehicles, the regular detection and control ·of physical, psychological and social deficiencies, additional protective measures, and the restriction of those who are.unfit to drive - are important measures to reduce traffic accidents.

Adequate functioning of vehicles (with statutory enforcement) and improved environmental conditions including traffic control and road conditions would likewise make a significant contribution. The level to which the occurrence and the toll of road accidents can be dropped is dependent on how effectively all the known factors are intercepted and upon interceptions of factors being applied concurrently.3

There are three levels of medical responsibility in terms of which these factors must be considered. The first level involves prevention of accidents and promotion of human knowledge, attitudes and practise in the stage of pre-pathogenesis (before injury, illness or abnormality). The second level involves care of accident victims, while at the third level the injured and maimed need to be rehabilitated in the community and work place.

The health professions hav.e largely 'been involved in diagnosing treatment and rehabilitative care due to the enormous toll from traffic accidents. Important social goals for individuals and· communities to focus upon would be - the production of vehicles geared towards safety rather than profits, the shift from the current one-person one car transport system towards a more efficient national, State subsidised transport system and the replacement of punitive measures for offenders towards one based upon re-education and service to the people.

'I

"" 122

4 BIBLIOGRAPHY

Statistical News Release : Summary of Road Traffic Accidents RSA 2 March 1984. Central Statistical Services. Pretoria 2 Epidemiological Comments Vol 9, No 9, September 1982. Department

~f Health and Welfare, Pretoria 3 Community Health - An Introductory Orientation for South African Students. I WF Spencer (1980) Shuter and Shooter, Pietermaritzburg ,.

Table 1. 123 MVA CASUALTY nATE PER 100 000 OF' TIlE ESTIMATED r'AID-YEAR II POPULATloN IN 1980 BY POPULA1' ION GROUP AND AGE.

:ill p 0 p r L A T I o X G nor P Group White Coloured ~ Black £Qlli 0 J,yrs. 153 167 124 '27 55 ; 9 2:;0 351 276 72 1:;1 10 - 14 367 358 378 ,151s ·219

15 19 1 616 583 691 257 :>--."., Zo - 24 1 636 854 916 335 61; 25 - 34 931 772 782 510 629 ,. 35 - 44 688 667 590 451 531 45 - 54 428 401 399 266 323 c:;- - ? an!] older 271 2S1 222 127 190

All ages 681 500 502 241 557 .------~---~------

ROAD TRAFFIC ACCIDENTS ALL ACCIDENTS 124 Figure 1 . 1 000

34 31 I '-./ 32 J~, ~. .~. 32 ~~ A \ I 'J \: !O ~ 30 g ~ ¥ 28 2S /"" "'I. ~G 25 e .. x( 24 'I 24 " " 21 22 1_\"" 22 .t..' ' , V~,, ,,J 20 \ , ~o \' I , I I , I I I I I I I I , I ,I n J 5 D n J 5 D n J 5 D n J 5 D n J 5 D 19/9 1980 1981 1982 1983

Figure 2 'PERSONS KILLED NUMBER

. ,~ ,-, ; " eoo ,. , , ena ~,." " r, ~ 4 ,"', " \ , I, , .! ,, ,, ' '.V ' , V ~- '_I " , '00 '00 I, I, " ," I, ;..J \ ...' 600 , W SO!) \1\ ,', ~ , Jf· I , I '\j:,. 500 ~" 500 ~ r-v', .,I , I ,, ,I , I \ . 400 • 400

I , I I I I . Ii' I I I I I , I I n.JSDnJSnnJSDnJSDnJSD 1979 1980 1981 1982 1983 Scale. Semi-Logarithmic Trend Cycle Seasonal~y Adjusted 125

J

UJ :I: I- ...... 0 ,i~ ...... ,.,... 0 ....'" 0 0 0 0 /':/ ~ ,,7 ... VI a::: '/ ' -:: !oJ c.. .l .. UJ 0 I- 00 <: C"I c::: ~ //', ~ /' >- c::: I- 0 ;/ ...J !J.. <: l . " UJ :::> :=-. :n <..? ./,/ AI: ,~ .<: <: ,./ ~/I ~" u I, Q - I- Z I,' Z <: UJ \ ~ UJ ":. \' c ( U .' \ \ 0 •.. f',,. U <: N ~ , U 0::- < >- u Cl \\\ u.. z - "\. \ u.. 0 \ VI , /$~I <: , c::: I- C!>, I- <: L.' ...J ~ ~' 0 < a... --i.' 0 0 1:..; 0:: a... I" o

\ \ : r\\"\\.\ ; \ : . \ : ~) '\,~,, \:- ____~ ______~ ,- 0 \: o o o o o o o o 8 o o C o o o o U) '" -7 (., c· CO "" ..:t 126

filure 4 , THE HORTALITY RATE I 100 000 POPULAl'TON AS A RESULT OF' MVAs

~y "STATUS" AND YEAR. REPUBLIC OF SOU.TH AFRICA, 1965 - 1975,

!;0

50 -;I I Overall ::1ortal i ty

til I ,.- .. _--.• ,- .. ------", ,_-0._-0-____ !:edal eyel ist!;

1965 65 &7 66 69 70 71 72 73 ill 75 7l~ 7i 78 127

DENTAL (ORAL) HEALni AND DISEASE

by M.H. Moolla Faculty of Dentistry University of the Western Cape 128

DENTAL (ORAL) HEALTH AND DISEASE

Oral Health)commonly known as .dental disease has little priority and perceptual importance'in the spectrum of diseases which afflict man. Paradoxically, the two ~ost co~on diseases which would afflict any individual in ,his or he~ lifetime would be dental caries and perio­ dontal di sease (i .e. gum disease). However, these di seases do not present themselves as life threatening afflictions which require immediate treatment or care.

4" ..'- DENTAL DISEASES

The two common dentai diseases which present any individual are dental caries and periodontal disease i.e: gum disease.

i) Dental Caries

a) Defi ni t ion

Dental caries in a laypersons' term is the rotting"of the teeth or tooth decay or dental cavities due to,the production . . of acids in the mouth from bacteriaa,nd plaque. Technically, one would describe dental decay or dental caries as a condi­ tion which affects only the teeth in the mouth which causes the demineralization of the teeth due to the production of acids from food debris and' bacteria .. The decay process takes place over a long period of time, anything from six months to couple of years depending upon the insult that ", has been. meted out to .the teeth due. to food' or neglect of the teeth. 129 Cavity extension Sinall pit cavity into dentin, Minimal tooth Extensive breakdown involvement of enamel -

Pulpal Missing Involvement tooth '"

b) Aetiology of dental caries

Basically the aetiology of dental caries is multifactorial but it is dependent on four essential factors which are modified by several contributory factors.

j

Principal faclors in che' dreay procts!i. il

I'I 130 \

In order for dental decay to be present the tooth has to be present which may be modified or affected from birth by various factors viz. genetics, calcium/phosphate metabolism, mineral deficiency etc. Also, the shape, size and form of each tooth will either encourage or discourage the bacteria (plaque) to demin ,~ra1ize the enamel of the tooth.

The second major aetio10gica1 factor is the microbacteria in the mouth which forms into clumps with -the saliva and mucus in the mouth to stick and adhere to the teeth surfaces producing harm­ ful _ acids to demineralize the teeth surfaces to cause ~ecay. This clumping of bacteria is called PLAQUE and forms like a thin, semi-transparent, sticky layer on the teeth surfaces. The plaque is not easily removed from the tooth surface unless some mechanical method like toothbrushing is used.

The plaque (and bacteria) derives most of its energy and source of energy from the type of food an individual eats. Therefore, the diet of the individual, is the third most important aetio­ logical factor for dental decay.

It is an accepted fact that .if we eat excessive amounts of re­ fined carbohydrates including large amounts of sugar, it would lead to greater tooth decay. The carbohydrates are easily broken down in the mouth to sucrose and fructose which help to support the bacteria (especially streptococcus mutans) to produce more acids. Hence resulting in repeated acid attacks on the enamel of the teeth. Foods most commonly assisting in the production of acid are refined carbohydrates like sweets, toffees, cakes, sweet confectionary, soft drinks, foods which contain hidden sugars like tomatoe ketchup, baked beans-etc. Almost 60% of processed foods available in the super­ markets contain some form of hidden sugar which is detrimental to dental health. ~f the food which is high in sugar content (called cariogenic diet) is continuously eaten over a long 1 131

period of time, and that the refined carbohydrates like sweets and toffees are eaten between me'a 1 times and if the nature of the refined carbohydrate like sticky toffees, sugared mebos," caramel remains' gl ued to the tooth surface for a long period of time, the decay process would be hastened.

To this must be added the additional factor that in third world countries a large percentage of the child population upto the age of 3-3~ years are exposed to sugared dri nks, very sweet tea 'or milk drink or 'a l'iquid sugared commercia) syrups which are supposed 'to be fortified with vitamins. Children given these drinks are exposed to' a common dental decay syndrome ca lled the baby bottle (nursi ng bottle) syndrome',

ii) PERIODONTAL DISEASE

a) Definition and Classification

The word "peri odonta 1" comes from the Greek, "peri '" whi ch means "around" and "odonto" which means "tooth". Since periodontal disease affects the tissues and membranes sl'rround the teeth, rather 'than the teeth themselves, the word ~ery accurately describes the nature of the disease' itsel f.

Periodontal 'disease (pyorrhea) can be described accurately in two 'very, broad stages, The initial and early state of

the disease is ca'lled gingivitis (gum disease or gum inflamma- ( tion). The disease is characterised by the infla'nination of the gums '~ith reddening, swelling and bleeding.

The advanced stage of periodontal disease called periodontitis (pyorr'hea) results in the formation of deep pockets between the gum and teeth, with destructi~n o'f surround i'ng bone of the teeth, loosening'of the teeth and eventually tooth loss. 132

Almost 95% of the total adult population in South Africa suffer from one form of periodontal disease or another during their ·life span. b) Aetiology of Periodontal Disease

The main cause of periodontal disease is persistent presence of plaque in the mouth. As described earlier plaque consist mainly of bacteria .which exceeds not only acid from furmentable carbohydrates but also produces bacterial toxins (poisons) which attack the gums and causes inflammation. The constant attack of bacterial toxins would lead' to affl iction of the underlying bone surround the gums and teeth leading to the formation of a space between gum and tooth called periodontal pocket.

The presence of plaque .in the mouth leads not only to destruct­ ion of the gums but the plaque would slowly mineralise to tartar Or calculus. The tartar or calculus is very hard and forms into greater quantity as more plaque accumulates and more minerals are absorbed from the saliva.

Chemically the tartar is similarly in composition as kidney stones, gallstones etc.

Besides plaque there are other contributory factors which causes gum disease namely the poor nutritional basis of the periodontal tissues, hormonal changes during pregnancy, and contracepti ve "Pi 11", certain drugs which cause greater production of connective tissue and in diseases like leukae­ mia, diabetes mellitus and vitamin deficiency. 133

c) Clinical Signs and Symptoms

The most common signs for gum disease may be described by: bleeding gums; gums very tender; receding gums with exposure of necks of teeth; bad breath; pus from the gums on pressure; loosing and mobility of teeth.

P"QU~CAl.CUUlS

gingival jnfl.-atlon

Spread of infl_lion .n4 Te.th btCOolle loo~e ,nd pockets ..,. exroli.t~

. Pt'riuduntal disl'USC.

PREVENTION OF DENTAL DISEASE )

Essentially there are four cardinal preventive measures for the control of dental decay and periodontal disease.

1) Diet Control

One needs to be .highly selective of the type of food one eats. Ideally one should refrain from foods which contain sugar or sucrose producing foods. From a practical point of view it would be best that one eats sugar containing foods at meal times after which one could brush ones teeth. To reduce the intake of snacks and sweets in between meals. 134

2) Oral Hygiene

i) To brush ones teeth after every meal in correct method. ii) To supplement the 'use of a multi-tufted toothbrush with a fluoride toothpaste. iii) To use additional methods of plaque removal like dental floss, dental tape and toothpicks.

3) Use of Fluorides

i ) Where possible to introduce systemic water fluoridation of community drinking water. To modify the level of drinking water so that it contains 1 mg of Fluoride ion in one litre of water. If this procedure is not possible then; ii) Fluoride tablets should be given to children from birth till the age of ~ 10 years. The dosage of fluoride tablet should be prescribed taking into account the level of fluoride in the water, the age and weight of the child and to check whether the child is not obtaining fluoride from any other sources. iii) In addition to this, each individual should brush his or her teeth with a fluoride containing toothpaste. iv) For children it is advocated that a fluoride mouthrinse programme should be operative. A forthnightly fluoride mouthrinse with 0.2% Sodium fluoride under supervision should be done.

'. All these methods indicate at least 30-60% reduction in dental decay .. It also helps in the reduction of bacterial toxins in the mouth thereby helping to control plaque. 135

4) Regular Check-up

It is advocated that patients see their dentist at regular intervals to check up for any dental disease. Considering that we use our mouth for almost everything we do like eating, speaking, singing; etc. we need to look after it.

How regularly one should go to the dentist would depend upon the nature of the disease process in one's mouth. If one shows • greater susceptibility to dental disease then one should see ones dentist more frequently. It is recommended that children see a dentist twice as frequently as adults. This is because the dentition in the childrens mouth is changing all the time from 0-12 years. Ideally, a child should see the dentist twice a year and an adult at least once a year.

CONCLUSION

Dental disease does not evoke the same spectre of emotions and energy amongst people as other diseases in the body. However, a large percentage of medical diseases manifest their signs in the mouth first . . For this reason alone, it would be important that health professionals and the population should not ignore the early signs of dental disease. For the often neglected gnawing tooth ache or bleeding gums may surrep­ tiously be the postends of some fatal disease,

Dental caries and periodontal disease are universal diseases affecting all nations of the world. The prevention of the diseases can be achieved by Simple preventi ve measures~ by brushing your teeth regularly, a good diet and use of fluorides. These papers constitute the preliminary findings of the Second Carnegie Inquiry into Poverty and Develop­ ment in Southern Africa, and were prepared for presen­ tation at a Conference at the University of Cape Town from 13-19 April, 1984. The Second Carnegie Inquiry into Poverty and Develop­ ment in Southern Africa was launched in April 1982, and is scheduled to run until June 1985. Quoting (in context) from these preliminary papers with due acknowledgement is of course allowed, but for permission to reprint any material, or for further infor­ mation about the Inquiry, please write to: SALDRU School of Economics Robert Leslie Building University of Cape Town Rondebosch 7700

Edina-Griffiths